Objective To construct the over-expressed lentivirus vector of PRDM5 gene and establish the Neuro-2a cells stably transfected PRDM5， and to provide the basis evidence for exploring the effect of PRDM5 in pathogenesis of ischemic stroke（IS）. Methods The sequence of PRDM5 was searched and designed based on NCBI. The PRDM5 gene was amplified by PCR and ligated with the lentiviral vector GV492 digested by BamHⅠ and AgeⅠ restriction enzymes to form the GV492-PRDM5 over-expression recombinant plasmid. The positive clones with similar length and size to the target gene fragment were screened by PCR and sent to Shenggong Bioengineering （Shanghai） Co. Ltd. for identification. The correctly-sequenced GV492-control plasmid and GV492-PRDM5 over-expression recombinant plasmid were transfected into the HEK293T cells， respectively. After 48 h of transfection， the lentiviruses were collected by centrifugation， and they were GV492-control lentivirus and GV492-PRDMS over-expression lentivirus； the titers of these two lentiviruses were determined by lentiviral titer assay. The Neuro-2a cells were divided into GV492-control group and GV492-PRDM5 group， and then infected with GV492-control lentivirus and GV492-PRDM5 over-expression lentivirus， respectively， with a lentivirus multiplicity of infection （MOI） of 100. The Neuro-2a cells successfully infected with GV492-control lentivirus and GV492-PRDM5 over-expression lentivirus were screened with puromycin （10 mg·L^-1） after 72 h of infection. The growth status and the expression of green fluorescence protein of Neuro-2a cells in GV492-control group and GV492-PRDM5 group were observed by fluorescence microscope. The expression levels of PRDM5 mRNA and PRDM5 protein in the Neuro-2a cells in two groups were detected by real-time fluorescence quantitative RCR（RT-qPCR） and Western blotting methods. Results The PCR results showed that the length of the positive transformant of GV492-PRDM5 recombinant plasmid was about 684 bp， and the gene sequence of GV492-PRDM5 over-expression recombinant plasmid was consistent with the designed and synthesized PRDM5 over-expression sequence. The titers of GV492-control lentivirus and GV492-PRDM5 over-expression lentivirus were both 2.5×10⁸ TU·mL^-1. The Neuro-2a cells in GV492-control group and GV492-PRDM5 group grew well， and the expressions of green fluorescence protein were found under fluorescence microscope.The RT-qPCR results showed that the expression level of PRDM5 mRNA in the Neuro-2a cells in GV492-PRDM5 group was significantly increased compared with GV492-control group（P<0.01）. The Western blotting results showed that the specific bands appeared in the Neuro-2a cells in GV492-control group and GV492-PRDM5 group with a relative molecular weight of 75 000； compared with GV492-control group， the expression level of PRDM5 protein in the Neuro-2a cells in GV492-PRDM5 group was increased（P<0.01）. Conclusion The over-expression lentivirus vector of PRDM5 gene is successfully constructed， and the stably transfected GV492-PRDM5-Neuro-2a cells are established.

Application of invisible orthodontic appliances in the treatment of adult skeletal malocclusions， especially in the cases requiring tooth extraction， has always been one of the challenges in invisible orthodontic technology. Our department received a 30-year-old female patient in March 2019； the patient presented with complaints of “crooked teeth and protruding mouth，” seeking orthodontic treatment to improve her facial profile. The patient had bilateral distal molar relationship， proclined maxillary and mandibular anterior teeth， and deep overjet； radiographic examination revealed an ANB angle of 6.2°， indicating a skeletal Class Ⅱ malocclusion. By extracting four first premolars and using four miniscrews， after 20 months of treatment， the extraction spaces were fully closed， the dental arch was aligned， and the occlusal relationship was favorable； the anterior teeth were retracted， the mandible showed a reverse rotation， and the soft tissue profile was significantly improved. Application of invisible orthodontic appliances in conjunction with miniscrews anchorage can achieve good three-dimensional control of tooth movement in adult extraction cases， providing a reference for clinical practitioners treating such patients.

Objective To discuss the protective effect of gingerone on the hippocampal neuron HT22 cells after oxygen-glucose deprivation/reoxygenation （OGD/R），and to clarify the related mechanism. Methods The HT22 cells were cultured， and the OGD/R cell injury model was established by setting the gradient of OGD/R time. The HT22 cells were divided into control group，OGD/R group， OGD/R+1 μmol·L^－1 gingerone group， OGD/R + 10 μmol·L^－1 gingerone group， OGD/R+100 μmol·L^－1 gingerone group，and OGD/R+0.2% dimethyl sulfoxide（DMSO） group.The viability of the cells in various groups was detected by CCK-8 assay； the survival rates of the cells in various groups were calculated to determine the optimal drug concentration of gingerone. The cells were divided into control， OGD/R group， OGD/R+ gingerone， and OGD/R+gingerone+nuclear factor erythroid-2-related factor 2（Nrf2） inhibitor（ML385） groups.The cells in OGD/R + gingerone group were treated with gingerone for 4 h before OGD treatment for 8 h followed by reoxygenation for 8 h， and the cells in OGD/R+gingerone+ML385 group were treated with 10 μmol·L^－1 ML385 for 6 h before gingerone treatment. The viability of the cells in various groups was detected by CCK-8 assay；the expression levels of Nrf2， heme oxygenase-1 （HO-1）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） proteins in the cells in various groups were detected by Western blotting method；the activity of superoxide dismutase （SOD） and the level of malondialdehyde （MDA） in the cell culture supernatant in various groups were detected by enzyme-linked immunosorbent assay （ELISA） method. Results Compared with control group， the survival rate of the HT22 cells was below 50% after treated with OGD for 8 h and reoxygenation for 8 h， so the HT22 cell OGD/R model was established by treated with OGD for 8 h and reoxygenation for 8 h. Compared with OGD/R group，the survival rates of the cells in OGD/R+different doses of gingerone groups were increased to various extents， and the survival rate of the cells in OGD/R+ 100 μmol·L^－1 gingerone group was significantly increased （P<0.01）； so 100 μmol·L^－1 gingerone was used for the subsequent experiment. Compared with control group， the viability of the cells in OGD/R group was significantly decreased （P<0.01）， and the expression levels of Nrf2， HO-1， and Bax proteins in the cells were significantly increased （P<0.01）， while the expression level of Bcl-2 protein in the cells was significantly decreased （P<0.05）， and the SOD activity in the cell culture supernatant was significantly decreased （P<0.01）， and the level of MDA was significantly increased （P<0.01）； compared with OGD/R group， the viability of the cells in OGD/R + gingerone group was significantly increased （P<0.01）， and the expression levels of Nrf2， HO-1， and Bcl-2 proteins in the cells were significantly increased （P<0.05 or P<0.01）， while the expression level of Bax protein in the cells was decreased（P<0.05）， the SOD activity in the cell culture supernatant was significantly increased （P<0.01）， and the level of MDA was significantly decreased （P<0.01）； compared with OGD/R + gingerone group， the viability of the cells in OGD/R + gingerone + ML385 group was significantly decreased （P<0.01）， and the expression levels of Nrf2， HO-1， and Bcl-2 proteins were significantly decreased （P<0.01）， while the expression level of Bax protein in the cells was significantly increased （P<0.01），the SOD activity in the cell culture supernatant was significantly decreased （P<0.01）， and the level of MDA was significantly increased （P<0.05）. Conclusion Gingerone alleviates the oxidative stress damage，and thereby plays an inhibiory effect on the apoptosis of the HT22 neurons by activating the Nrf2/HO-1 signaling pathway after OGD/R.

目的：探讨双酚A （BPA）对子宫内膜间充质干/基质细胞（eMSCs）增殖活性和干性特征的影响，阐明人脐带间充质干细胞源性上清（hUCMSC-Sup）对细胞损伤的改善作用。方法：体外培养eMSCs，以0、200、250、300、350、400μmol·L^-1 BPA处理。将eMSCs分为对照组（仅培养液培养）、BPA组(含200μmol·L^-1 BPA的等体积培养液培养)、 BPA+hUCMSC-Sup组(含200μmol·L^-1 BPA及50%体积比hUCMSC-Sup的等体积培养液培养)和BPA+CHIR-99021组(含200μmol·L^-1 BPA及10μmol·L^-1 CHIR-99021的等体积培养液培养)，使用干细胞成球培养液培养eMSCs干细胞球，其余细胞均使用DMEM/F12完全培养基培养。噻唑蓝（MTT）法检测各组eMSCs存活率，球体形成实验检测各组eMSCs干细胞球数和直径，CCK-8法检测各组eMSCs干细胞球中细胞增殖活性，流式细胞术检测各组eMSCs中CD73+细胞百分率，实时荧光定量PCR（RT-qPCR）法检测各组eMSCs中性别决定区Y框蛋白2（Sox2）、八聚体结合转录因子4 （Oct4）和Nanog mRNA表达水平，Western blotting法检测各组eMSCs中β-连环蛋白（β-catenin）蛋白表达水平。结果：MTT法检测，BPA作用24和48 h，与0μmol·L^-1 BPA组比较，200、250、300、350和400μmol·L^-1 BPA组eMSCs存活率均明显降低（P<0.01）。药物作用24 h时，与对照组比较，BPA组eMSCs存活率明显降低（P<0.01）；药物作用48 h时，与对照组比较，BPA组eMSCs存活率明显降低（P<0.01）；与BPA组比较，BPA+hUCMSC-Sup组eMSCs存活率明显升高（P<0.05）。球体形成实验检测，与培养3 d组比较，培养4和5 d组eMSCs干细胞球数和直径均明显增加（P<0.05或P<0.01）；与对照组比较，培养48 h时BPA组eMSCs干细胞球数和直径均明显减少（P<0.05或P<0.01）。CCK-8法检测，处理24和48 h时，与对照组比较，BPA组eMSCs干细胞球中细胞增殖活性均明显降低（P<0.01）；与BPA组比较，BPA+hUCMSC-Sup组eMSCs干细胞球中细胞增殖活性均明显升高（P<0.01）。流式细胞术检测，与对照组比较，BPA组eMSCs中CD73+细胞百分率明显降低（P<0.01）；与BPA组比较，BPA+hUCMSC-Sup组eMSCs中CD73+细胞百分率明显升高（P<0.01）。RT-qPCR法检测，与对照组比较，BPA组eMSCs中Sox2、Oct4和Nanog mRNA表达水平均明显降低（P<0.01）；与BPA组比较，BPA+hUCMSC-Sup组和BPA+CHIR-99021组eMSCs中Sox2、Oct4及Nanog mRNA表达水平均明显升高（P<0.01）。Western blotting法检测，与对照组比较，BPA组eMSCs中β-catenin蛋白表达水平明显降低（P<0.01）；与BPA组比较，BPA+hUCMSC-Sup组和BPA+CHIR-99021组eMSCs中β-catenin蛋白表达水平均明显升高（P<0.01）。结论：BPA能够抑制eMSCs的干性特征，损伤子宫内膜的自我更新及修复作用，其机制可能与下调细胞中Wnt/β-catenin信号通路活性有关。hUCMSC-Sup可以促进受损eMSCs的增殖，并对BPA诱导的eMSCs干性损伤起到改善作用。

Objective To investigate the efficacy and safety of fospropofol disodium （FP） in the induction and maintenance of general anesthesia in the adult patients graded Ⅰ or Ⅱ by the American Society of Anesthesiologists （ASA） undergoing elective surgery， and to provide the theoretical basis for application of EP in the induction and maintenance of general anesthesia. Methods Adult patients of ASA grade Ⅰ or Ⅱ undergoing elective surgery were selected with a total of 100 patients recruited sequentially according to the time of visit， and they were randomly divided into FP group （50 cases） and propofol group （50 cases）. All patients were prepared preoperatively， and received a slow injection of midazolam （2 to 3 mg） and sufentanil （0.3 μg·kg^-1）， followed by induction of anaesthesia 1 to 2 min later. The patients in FP group were given FP （10.0-12.5 mg·kg^-1） intravenously， and the patients in propofol group were given propofol （1.5-2.0 mg·kg^-1） intravenously. After the Modified Obserational Assessment Alertness/Sedation （MOAA/S） score dropped to 1， muscle relaxant was administrated and the induction was completed. During the maintenance of anaesthesia， the patients in FP group received a continuous intravenous infusion of FP at a rate of 12.5-15.0 mg·kg^-1·h^-1， and the patients in propofol group received a continuous infusion of propofol at a starting rate of 6 mg·kg^-1·h^-1. The patients in two groups additionally received remifentanil （0.1-0.4 μg·kg^-1·min^-1） for co-analgesia， and the rate of administration was adjusted according to the patient’s status. Systolic blood pressure （SBP）， diastolic blood pressure （DBP）， mean arterial pressure （MAP）， heart rate （HR） and bispectral index （BIS） values of the patients in two groups were recorded at different time points： before induction （T₁）， immediately after tracheal intubation （T₂）， 5 min after induction （T₃）， 10 min after induction （T₄）， 20 min after induction （T₅）， 30 min after induction （T₆）， 40 min after induction （T₇） and at the end of the procedure （T₈）. The time to onset of sedation/anaesthesia （MOAA/S≤1）， the time to eye opening， and the time to awakening （MOAA/S=5） of the patients in two groups were recorded. The lowest intraoperative SBP and BIS values and the time required of the patients in two groups were observed. The incidence of adverse reactions related to agitation， choking， nausea， vomiting and cardiovascular system or respiratory system were compared between two groups. Results There were no statistically differences in the general informations and the duration of surgery of patients between two groups （P>0.05）. The induction time of the patients in FP group （2.39 min） was significantly longer than that in propofol group （0.70 min） （P<0.05）. In the recovery period of general anesthesia， the eye opening time and recovery time of the patients in FP group were significantly longer than those in propofol group （P<0.05）. There were no significant differences in MAP of the patients between two groups at different time points （P>0.05）. The HR at T₄， T₅， T₆， and T₇ time points of the patients in FP group were lower than those in propofol group （P<0.05）. The lowest value of BIS of the patients in FP group was significantly smaller than that in propofol group， and the time taken to reach the lowest value of BIS in FP group was significantly longer than that in propofol group （P<0.05）. The time taken to reach the lowest value of SBP of the patients in FP group was longer than that in propofol group （P<0.05）. However， the lowest value of SBP of the patients and the incidence of adverse reations of the patients in two groups showed no statistical differences （P>0.05）. Conclusion Compared with propofol， FP injection is safe and effective in the induction and maintenance of general anesthesia in adult patients with ASA class Ⅰ or Ⅱ undergoing elective surgery， with a low incidence of adverse reactions， which is a new anesthesia option.

Objective To discuss the effect of apolipoprotein C1 （APOC1） expression on the proliferation and apoptosis of the hepatocellular carcinoma cells， and to preliminarily clarify the related molecular mechanism. Methods The expression level of APOC1 mRNA in hepatocellular carcinoma tissue and its relationship with the prognosis of the patient were analyzed by The Cancer Genome Atlas （TCGA） Database； real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the expression levels of APOC1 mRNA in different hepatocellular carcinoma cells； the human liver cancer HepG2 cells with low APOC1 expression were selected as the subjects. The HepG2 cells were transfected with pcDNA3.1-APOC1 plasmid to over-express APOC1 （APOC1 over-expression group），and the HepG2 cells transfected with empty vector pcDNA3.1 were regarded as control group. MTS assay and 5-ethynyl-2'-deoxyuridine （EdU） staining were used to detect the proliferative activities and proliferation rates of the cells in two groups； Transwell chamber assay was used to detect the numbers of migration cells in two groups；flow cytometry and TUNEL assay were used to detect the percentages of the cells at different cell cycles and apoptotic rates in two groups；Western blotting method was used to detect the expression levels of extracellular regulated protein kinase （ERK）， phosphorylated ERK （p-ERK）， protein kinase B （AKT）， phosphorylated AKT （p-AKT）， B-cell lymphoma-2 （Bcl-2）， and cleaved cysteinyl aspartate specific proteinase-3（cleaved caspase-3） proteins in the cells in two groups. Results The TCGA Database results showed that the expression level of APOC1 mRNA in hepatocellular carcinoma tissue was lower than that in normal liver tissue （P<0.05）， and the patients with low expression of APOC1 mRNA had poor prognosis. The RT-qPCR results showed that the expression level of APOC1 mRNA in the HepG2 cells was the lowest， and the HepG2 cells were chosen for the subsequent research. Compared with control group， the proliferative activity and proliferation rate of the cells in APOC1 over-expression group were decreased （P<0.05 or P<0.01），the number of migration cells was decreased （P<0.01），and the percentage of the cells at S phase and the apoptotic rate were significantly increased （P<0.01）. Compared with control group， the expression levels of p-ERK， p-AKT， and Bcl-2 proteins in the cells in APOC1 over-expression group were significantly decreased （P<0.05），and the expression level of cleaved caspase-3 protein was increased （P<0.01）. Conclusion High expression of APOC1 can inhibit the proliferation of the human liver cancer HepG2 cells and induce the apoptosis，and its mechanism may be related to inhibition of the expressions of p-ERK，p-AKT，Bcl-2 proteins and promotion of the expression of cleaved caspase-3 protein.

Objective To discuss the effect of downregulating of high mobility group box protein 2 （HMGB2） expression on the biological behavior of the liver cancer cells and the epithelial-mesenchymal transition （EMT） process， and to clarify its mechanism. Methods The human liver cancer LM3 cells at logarithmic growth phase were divided into negative control group and HMGB2 RNA interference group （HMGB2 siRNA group）；the cells in two groups were transfected with RNA oligonucleotides（RNA oligos） with irrelevant sequences and RNA oligos designed to knock down HMGB2， and the Lipofectamine 2000 was regarded as the vector.The expression levels of HMGB2 mRNA and protein in the cells in two groups were detected by real-time fluorescence quantitative PCR （RT-qPCR） and Western blotting methods； cell scratch assay and Transwell chamber assay were used to detect the migration and invasion abilities of the cells in two groups； the expression levels of E-cadherin， N-cadherin， and Vimentin proteins and protein kinase B （AKT）/mammalian target of rapamycin （mTOR） pathway related proteins in the cells in two groups were detected by Western blotting method. Results Compared with negative control group， the expression levels of HMGB2 mRNA and protein in the cells in HMGB2 siRNA group were significantly decreased （P<0.05），the cell scratch healing rate was significantly decreased （P<0.01），the number of invasion cells was significantly decreased （P<0.01），and the expression level of E-cadherin protein in the cells was significantly increased （P<0.01）， while the expression levels of N-cadherin， Vimentin， mTOR， AKT， and phosphorylated AKT （p-AKT） proteins in the cells were significantly decreased （P<0.05 or P<0.01）. Conclusion Downregulating the expression of HMGB2 can reduce the migration and invasion abilities of the liver cancer LM3 cells and inhibit the EMT，and its mechanism may be related to regulating the expression of the AKT/mTOR pathway related proteins.

目的：探讨小白菊内酯（PTL）通过调控机械敏感性离子通道蛋白1 （Piezo1）表达对机械牵张应力作用下软骨细胞凋亡的影响，并阐明其相关作用机制。方法：按照拉伸性变量将软骨细胞分为0%、5%、10%、15%和20%拉伸组。另取软骨细胞，分为对照组、20%拉伸组、20%拉伸+5μmol·L^-1 PTL组、20%拉伸+10μmol·L^-1 PTL组和20%拉伸+20μmol·L^-1 PTL组。使用Piezo1短发夹RNA （shRNA）干扰慢病毒（sh-Piezo1）或shRNA-NC慢病毒感染软骨细胞，将软骨细胞分为sh-Piezo1组和sh-NC组，另设置空白对照组。另将软骨细胞分为20%拉伸组、20%拉伸+PTL组、20%拉伸+sh-Piezo1组和20%拉伸+sh-Piezo1+PTL组。Hoechst 33258荧光染色观察各组细胞核形态表现，流式细胞术检测各组细胞凋亡率，分光光度法检测各组细胞中含半胱氨酸的天冬氨酸蛋白酶（Caspase）-3活性，CCK-8法检测各组细胞增殖率，Fluo-4/AM荧光探针法检测各组细胞中钙离子(Ca²⁺)水平，实时荧光定量PCR （RT-qPCR）法检测各组细胞中Piezo1 mRNA表达水平，Western blotting法检测各组细胞中Piezo1蛋白表达水平。结果：Hoechst 33258荧光染色观察，随着拉伸量逐渐增加，0%、5%、10%、15%和20%拉伸组软骨细胞细胞核呈碎块状致密浓染的软骨细胞数量逐渐增加。流式细胞术检测，与0%拉伸组比较，5%、10%、15%和20%拉伸组软骨细胞凋亡率均明显升高（P<0.01）；与对照组比较，20%拉伸组软骨细胞中细胞凋亡率明显升高（P<0.05）；与20%拉伸组比较，20%拉伸+5μmol·L^-1 PTL组、 20%拉伸+10μmol·L^-1 PTL组和20%拉伸+20μmol·L^-1 PTL组软骨细胞细胞凋亡率均明显降低（P<0.05）；与20%拉伸组比较，20%拉伸+PTL组和20%拉伸+sh-Piezo1组软骨细胞凋亡率均明显降低（P<0.05）。分光光度法检测，与0%拉伸组表示，5%、10%、15%和20%拉伸组软骨细胞中Caspase-3活性均明显升高（P<0.01）；与对照组比较，20%拉伸组软骨细胞中Caspase-3活性明显升高（P<0.05）；与20%拉伸组比较，20%拉伸+5μmol·L^-1 PTL组、20%拉伸+10μmol·L^-1 PTL组和20%拉伸+20μmol·L^-1 PTL组软骨细胞中Caspase-3活性均明显降低（P<0.05）；与20%拉伸组比较，20%拉伸+PTL组和20%拉伸+sh-Piezo1组软骨细胞中Caspase-3活性均明显降低（P<0.05）。CCK-8法检测，与0μmol·L^-1 PTL组比较，40.00、 80.00和160.00μmol·L^-1 PTL组软骨细胞增殖率均明显降低（P<0.05），提示20.00μmol·L^-1 PTL为最高无毒性作用浓度。Fluo-4/AM荧光探针法检测，与对照组比较，20%拉伸组软骨细胞中Ca²⁺水平明显升高（P<0.05）；与20%拉伸组比较，20%拉伸+5μmol·L^-1 PTL组、20%拉伸+10μmol·L^-1 PTL组和20%拉伸+20μmol·L^-1 PTL组软骨细胞中Ca²⁺水平均明显降低（P<0.05）；与20%拉伸组比较，20%拉伸+PTL组和20%拉伸+sh-Piezo1组软骨细胞中Ca²⁺水平均明显降低（P<0.05）。RT-qPCR法检测，与空白对照组和sh-NC组比较，sh-Piezo1组软骨细胞中Piezo1 mRNA表达水平明显降低（P<0.05）。Western blotting法检测，与对照组比较，20%拉伸组软骨细胞中Piezo1蛋白表达水平明显升高（P<0.05）；与20%拉伸组比较，20%拉伸+5μmol·L^-1PTL组、20%拉伸+10μmol·L^-1 PTL组和20%拉伸+20μmol·L^-1 PTL组软骨细胞中Piezo1蛋白表达水平均明显降低（P<0.05）；与空白对照组和sh-NC组比较，sh-Piezo1组软骨细胞中Piezo1蛋白表达水平明显降低（P<0.05）。结论：PTL可抑制高强度周期性机械牵张应力诱导的软骨细胞凋亡，其作用机制可能与抑制Piezo1介导Ca²⁺内流引起的细胞凋亡有关。

目的：探讨扶正软坚抗癌方调控蛋白激酶B （Akt）/鼠双微体2 （MDM2）/P53信号通路对肝癌HepG2细胞恶性生物学行为的影响。方法：采用0、0.05、0.10、0.20、0.40、0.80、1.60、3.20和6.40 g·mL^-1扶正软坚抗癌方分别处理HepG2细胞48 h,CCK-8法检测HepG2细胞存活率，筛选扶正软坚抗癌方浓度用于后续实验。将HepG2细胞分为对照组、低剂量扶正软坚抗癌方组(0.2 g·mL^-1)、中剂量扶正软坚抗癌方组(0.4 g·mL^-1)、高剂量扶正软坚抗癌方组(0.8 g·mL^-1)、SC79组(8 mg·L^-1 SC79)和高剂量扶正软坚抗癌方+SC79组(0.8 g·mL^-1扶正软坚抗癌方+8 mg·L^-1 SC79)。CCK-8法检测各组HepG2细胞增殖活性，克隆形成实验检测各组HepG2细胞克隆形成率，流式细胞术检测各组HepG2细胞凋亡率，Transwell小室实验检测各组HepG2细胞迁移和侵袭细胞数，Western blotting法检测各组HepG2细胞中增殖细胞核抗原（PCNA）、含半胱氨酸的天冬氨酸蛋白酶3 （Caspase-3）、基质金属蛋白酶（MMP）-2、MMP-9、磷酸化Akt （p-Akt）、磷酸化MDM2（p-MDM2）和P53蛋白表达水平。结果：随着扶正软坚抗癌方浓度(0、0.05、0.10、0.20、0.40、0.80、 1.60、 3.20和6.40 g·mL^-1)的升高，HepG2细胞存活率逐渐降低（P<0.05），选取0.2、0.4和0.8 g·mL^-1扶正软坚抗癌方用于后续实验。CCK-8法检测，与对照组比较，低、中和高剂量扶正软坚抗癌方组HepG2细胞增殖活性均明显降低（P<0.05），并呈剂量依赖性，SC79组HepG2细胞增殖活性明显升高（P<0.05）；与高剂量扶正软坚抗癌方组比较，高剂量扶正软坚抗癌方+SC79组HepG2细胞增殖活性明显升高（P<0.05）。克隆形成实验检测，与对照组比较，低、中和高剂量扶正软坚抗癌方组HepG2细胞克隆形成率均明显降低（P<0.05），并呈剂量依赖性，SC79组HepG2细胞克隆形成率明显升高（P<0.05）；与高剂量扶正软坚抗癌方组比较，高剂量扶正软坚抗癌方+SC79组HepG2细胞克隆形成率明显升高（P<0.05）。流式细胞术检测，与对照组比较，低、中和高剂量扶正软坚抗癌方组HepG2细胞凋亡率均明显降低（P<0.05），并呈剂量依赖性，SC79组HepG2细胞凋亡率明显升高（P<0.05）；与高剂量扶正软坚抗癌方组比较，高剂量扶正软坚抗癌方+SC79组HepG2细胞凋亡率明显升高（P<0.05）。Transwell小室实验检测，与对照组比较，低、中和高剂量扶正软坚抗癌方组HepG2细胞迁移和侵袭细胞数均明显降低（P<0.05），并呈剂量依赖性，SC79组HepG2细胞迁移和侵袭细胞数均明显升高（P<0.05）；与高剂量扶正软坚抗癌方组比较，高剂量扶正软坚抗癌方+SC79组HepG2细胞迁移和侵袭细胞数均明显升高（P<0.05）。Western blotting法检测，与对照组比较，低、中和高剂量扶正软坚抗癌方组HepG2细胞中PCNA、MMP-2、MMP-9、p-Akt和p-MDM2蛋白表达水平均明显降低（P<0.05），并呈剂量依赖性；Caspase-3和P53蛋白表达水平均明显升高（P<0.05），并呈剂量依赖性；SC79组HepG2细胞中PCNA、MMP-2、MMP-9、p-Akt和p-MDM2蛋白表达水平均明显升高（P<0.05）, Caspase-3和P53蛋白表达水平均明显降低（P<0.05）；与高剂量扶正软坚抗癌方组比较，高剂量扶正软坚抗癌方+SC79组HepG2细胞中PCNA、MMP-2、MMP-9、p-Akt和p-MDM2蛋白表达水平均明显升高（P<0.05）,Caspase-3和P53蛋白表达水平均明显降低（P<0.05）。结论：扶正软坚抗癌方抑制HepG2细胞增殖、迁移和侵袭，促进细胞凋亡，其作用机制与抑制Akt/MDM2信号通路、上调P53蛋白表达有关。

Objective To discuss the effect of NOD-like receptor protein 3 （NLRP3） inflammasome on the renal interstitial fibrosis in the unilateral ureteral obstruction （UUO） model rats， and to clarify its potential mechanism. Methods Thirty healthy male Wistar rats were randomly divided into sham operation group （n=6） and UUO group （n=24）. The rats in sham operation group underwent the dissection of the ureter without ligation， while the rats in UUO group were sacrificed on the 3rd， 7th， and 14th days after operation， and based on the treatment duration，the rats were divided into UUO 3 d group （n=8）， UUO 7 d group （n=8）， and UUO 14 d group （n=8）. HE staining and Masson staining were used to observe the pathomorphology of kidney tissue of the rats in various groups； reagent kits were used to detect the levels of malondialdehyde （MDA）， activities of superoxide dismutase （SOD）， and levels of hydroxyproline （HYP） in kidney tissue of the rats in various groups；immunohistochemistry method was used to detect the expression levels of α-smooth muscle actin （α-SMA） and transforming growth factor-β1 （TGF-β1） proteins in kidney tissue of the rats in various groups； Western blotting method was used to detect the expression levels of NLRP3 protein in kidney tissue of the rats in various groups. Results The HE staining results showed significant tubular dilation， interstitial edema， and widening， with increased infiltration of inflammatory cells， and shedding of epithelial cells was seen in parts of the tubular lumina of the rats in UUO group. Compared with sham operation group， the interstitial fibrosis scores of the rats in UUO 3 d， UUO 7 d， and UUO 14 d groups were significantly increased （P<0.05）； compared with UUO 3 d group and UUO 7 d group， the interstitial fibrosis score of the rats in UUO 14 d group was significantly decreased （P<0.05）. The Masson staining results showed that in UUO group， there was evident infiltration of inflammatory cells in the renal interstitium and a noticeable increase in fibrotic tissue proliferation； with the increasing of duration of UUO， some tubular structures disappeared， and the interstitial widened further with gradually increasing collagen deposition， particularly at the corticomedullary junction. Compared with sham operation group， the interstitial fibrosis scores of the rats in UUO 3 d， UUO 7 d， and UUO 14 d groups were significantly increased （P<0.05）； and compared with UUO 3 d and UUO 7 d groups， the interstitial fibrosis score of the rats in UUO 14 d group was significantly decreased （P<0.05）. Compared with sham operation group， the levels of MDA in obstructed kidney tissue of the rats in UUO 3 d， UUO 7 d， and UUO 14 d groups were significantly increased （P<0.05）， and the SOD activities were significantly decreased （P<0.05）. Compared with sham operation group， the levels of HYP in obstructed kidney tissue of the rats in UUO 3 d， UUO 7 d， and UUO 14 d groups were also significantly increased （P<0.05）；compared with UUO 3 d group， the level of HYP in obstructed kidney tissue of the rats in UUO 14 d group was significantly increased （P<0.05）. The immunohistochemistry results showed that compared with sham operation group， the expression levels of α-SMA protein in kidney tissue of the rats in UUO 3 d， UUO 7 d， and UUO 14 d groups were significant increased （P<0.05）； compared with UUO 3 d and UUO 7 d groups， the expression levels of α-SMA protein in kidney tissue of the rats in UUO 14 d group was significantly increased （P<0.05）； compared with sham operation group，the expression levels of TGF-β1 protein in renal tubular epithelial cells and renal tubule interstitial tissue of the rats in UUO 3 d， UUO 7 d， and UUO 14 d groups were also significantly increased （P<0.05）； compared with UUO 3 d group， the expression levels of TGF-β1 protein in the tubular epithelial cells and renal tubule interstitial tissue of the rats in UUO 14 d group were significantly decreased（P<0.05）. The Western blotting results showed that compared with sham operation group， the expression levels of NLRP3 protein in kidney tissue of the rats in UUO 7 d and UUO 14 d groups were significantly increased （P<0.05）. Conclusion The NLRP3 inflammasome plays a critical role in renal fibrosis of the UUO rats，and its mechanism may be related to the increasing of oxidative stress and the increasing of expression level of TGF-β1 protein.

Objective To discuss the effect of asiatic acid （AA） on the inflammation and oxidative stress damage induced by lipopolysaccharide （LPS） in the primary cultured hippocampus neurons， and to clarify its mechanism. Methods The primary cultured rat hippocampus neurons （cell purity identified by immunofluorescence staining） were divided into control group， LPS （10 mg·L^-1） group， and LPS+AA group （10 mg·L^-1 LPS+10， 20， and 40 µmol·L^-1 AA）， AA group （20 µmol·L^-1 AA）， ML385 group ［10 µmol·L^-1 nuclear factor erythroid 2-related factor （Nrf2） inhibitor］， and LPS+ML385+AA group （10 mg·L^-1 LPS+10 µmol·L^-1 ML385+20 µmol·L^-1 AA）. After drug treatment， methylthiazolyldiphenyl-tetrazolium bromide （MTT） method was used to detect the survival rates of the hippocampus neurons in various groups； lactate dehydrogenase （LDH） kit was used to detect the LDH leakage rates of the hippocampus neurons in various groups； enzyme linked immunosorbent assay （ELISA） kit was used to detect the expression levels of inflammatory factors ［interleukin （IL）-1β and tumor necrosis factor （TNF）-α］ and the activities of superoxide dismutase （SOD） and malondialdehyde （MDA） levels in the hippocampus neurons in various groups； Griess method was used to detect the nitric oxide （NO） levels in supernatant of the hippocampus neurons in various groups； immunofluorescence staining was used to detect the expressions of Nrf2 and heme oxygenase-1 （HO-1） proteins in the hippocampus neurons in various groups； Western blotting method was used to detect the expression levels of Nrf2， HO-1， nuclear factor-kappa B（NF-κB）， and B-cell lymphoma 2 （Bcl-2） proteins in the hippocampus neurons in various groups. Results Compared with control group， the survival rate of the hippocampus neurons， SOD activity， and Bcl-2 expression level in the cells in LPS group were significantly decreased （P<0.01）， while the LDH leakage rate， expression levels of IL-1β and TNF-α， MDA level， and NO level， as well as the expression level of NF-κB protein， were significantly increased （P<0.01）； the fluorescence intensities and expression levels of Nrf2 and HO-1 proteins in hippocampus neurons were significantly decreased （P<0.01）. Compared with LPS group， the survival rates of hippocampus neurons， SOD activities， and expression levels of Bcl-2 in the cells in LPS+10 µmol·L^-1 AA group and 20 µmol·L^-1 AA group were significantly increased （P<0.01）， while the LDH leakage rates， expression levels of IL-1β and TNF-α， MDA levels， and NO levels， as well as expression levels of NF-κB protein， were significantly decreased （P<0.05 or P<0.01）， and the fluorescence intensities and protein expression levels of Nrf2 and HO-1 in the cells were significantly increased （P<0.01）. Compared with LPS+20 µmol·L^-1 AA group， the fluorescence intensities of Nrf2 and HO-1 in the cells in LPS+ML385+AA group were significantly decreased （P<0.01）， and the expression levels of Nrf2 protein in the nucleus and cytoplasm， the expression levels of HO-1 and Bcl-2 proteins in the cells were significantly decreased （P<0.01）， while the expression level of NF-κB protein was significantly increased （P<0.01）. Conclusion AA can improve LPS-induced inflammation and oxidative stress damage in the primary cultured rat hippocampus neurons， and its mechanism may be related to the activation of the Nrf2/HO-1 signaling pathway.

Objective To clone the Helicobacter pylori （Hp） hp0169 gene and conduct the crystallographic study， and to clarify its secondary and tertiary structures. Methods The hp0169 gene and its encoded protein sequence of the Hp NCTC26695 strain were retrieved from the UniProt database. Bioinformatics method was used to analyze the physicochemical properties of the Hp recombinant protease （HpPrtC） protein； SOPMA and DNAStrar softwares were used to predict the secondary structure characteristics of HpPrtC protein； SWISS-MODEL software was used to construct the tertiary structure of the HpPrtC protein； IEDB and ABCpred softwares were used to predict the antigenic epitopes of the B lymphocytes HpPrtC protein； SYFPEITMI website was used to predict the antigenic epitopes of the T lymphocytes of HpPrtC protein； the expert pool （EP） and random forest （RF） algorithms were used to predict the crystallizability of the HpPrtC protein；the HpPrtC recombinant protein was expressed in the prokaryotic system； the HpPrtC recombinant protein was purified by Ni²⁺ affinity chromatography and size-exclusion chromatography；the crystallization conditions for HpPrtC were screened by crystallization kit. Results The hp0169 gene contained 1 269 base pairs and encoded the protein of 422 amino acids， the theoretical isoelectric point was 7.64 and the relative molecular weight was 47 300. HpPrtC was a hydrophilic and soluble protein. The number of amino acids of alpha helices of HpPrtC accounted for 35.78%， beta sheets 18.72%， beta turns 6.87%， and random coils 38.63%. The antigen epitope analysis results showed that HpPrtC contained five dominant linear epitopes of B lymphocytes， three conformational epitopes， and multiple potential dominant epitopes of T lymphocytes. The homology modeling results showed that HpPrtC formed a dimer， and each monomer displayed a barrel structure surrounded by β sheets， alpha helices， and random coils. HpPrtC was predicted to have moderate crystallizability without signal peptides and transmembrane helices. Small clustered needle-like crystals of HpPrtC were obtained under the conditions of 0.2 mol·L^-1 magnesium chloride， 0.1 mol·L^-1 tris （hydroxymethyl） amino methane（Tris）， 3.4 mol·L^-1 hexanediol， and pH=8.5. Conclusion HpPrtC is a hydrophilic protein that forms a dimeric structure and crystallizes into small clustered needle-like crystals under suitable conditions. HpPrtC contains dominant antigenic epitopes of the T lymphocytes and B lymphocytes and can serve as an antigen for the design of Hp vaccines to establish the multivalent fusion vaccines or multi-epitope vaccines； the results provide an experimental basis for the prevention and control of Hp.

目的：探讨罗伊氏乳杆菌对轮状病毒（RV） SA11株体内外复制的抑制作用，并阐明其对相关免疫因子表达的影响。方法：体外实验，培养并鉴定罗伊氏乳杆菌，绘制罗伊氏乳杆菌标准曲线和生长曲线，筛选罗伊氏乳杆菌培养最佳时间和最适浓度。采用5×10～8、10×10～8、50×10～8、100×10～8、200×10～8和500×10～8 CFU·mL^-1罗伊氏乳杆菌感染细胞，台盼蓝染色法检测Caco-2细胞存活率。将不同浓度罗伊氏乳杆菌与RV体外共孵育并作用于Caco-2细胞，Caco-2细胞分为阴性对照组（NC组）、阳性对照组（PC组）和10～7、10～8、10～9及10¹⁰ CFU·mL^-1罗伊氏乳杆菌组，免疫荧光灶法检测罗伊氏乳杆菌作用后Caco-2细胞中病毒滴度，实时荧光定量PCR （RT-qPCR）法检测不同浓度罗伊氏乳杆菌作用后Caco-2细胞中RV VP6基因拷贝数。体内实验，将25窝SPF级乳鼠分为对照组、RV组（感染SA11毒株）、Ab-NC组（抗生素处理耗竭肠道菌群）、Ab-RV组（耗竭肠道菌群后感染SA11毒株）和Ab-Lac-RV组（耗竭肠道菌群，并感染罗伊氏乳杆菌后感染SA11毒株）。收取各组乳鼠灌胃第2、4、6、8和10天的粪便样本和灌胃第4天结肠组织样本，RT-qPCR法检测各组乳鼠粪便中RV VP6基因拷贝数和结肠组织中白细胞介素（IL）-1β、IL-8、IL-10、γ干扰素（IFN-γ）和肿瘤坏死因子（TNF）-αmRNA表达水平。结果：罗伊氏乳杆菌生长良好，形态圆润，呈圆形、光滑和乳白色的凸起样菌落，且边缘较整齐；革兰染色后菌体呈紫色、不规则和方形杆状；经16SrDNA测序后序列同源性为99%，提示罗伊氏乳杆菌活化成功；罗伊氏乳杆菌活菌数与吸光度（A）值呈线性关系，回归分析标准曲线为Y=0.437 5X+0.000 6,R2=0.999 4。培养0～2 h，细菌处于对数生长期，细菌生长迟缓；培养2～14 h，细菌快速生长，并于培养14～16 h时细菌生长趋于稳定，培养16 h时达到细菌生长速率顶峰，随后进入衰亡期。5×10～8、10×10～8、50×10～8、100×10～8和200×10～8 CFU·mL^-1罗氏乳杆菌感染后，Caco-2细胞存活率均>90%，因此选用上述浓度罗氏乳杆菌感染细胞。与PC组比较，5×10～8、10×10～8、50×10～8、100×10～8和200×10～8 CFU·mL^-1罗氏乳杆菌组Caco-2细胞中RV VP6基因拷贝数均明显降低（P<0.01）。与PC组比较，10～7、10～8、10～9和10¹⁰ CFU·mL^-1罗伊氏乳杆菌组Caco-2细胞中病毒滴度均明显降低（P<0.01）。与对照组比较，Ab-NC组、Ab-RV组和Ab-Lac-RV组乳鼠肠道菌群菌落数量均明显减少，乳鼠肠道菌群耗竭成功。灌胃第2和4天，与RV组比较，Ab-RV组乳鼠粪便中RV VP6基因拷贝数明显降低（P<0.05）；灌胃第4、6、8和10天，与Ab-RV组比较，Ab-Lac-RV组乳鼠粪便中RV VP6基因拷贝数明显降低（P<0.05）。与对照组比较，Ab-RV组和Ab-Lac-RV组乳鼠结肠组织中IL-1β、IL-10、IFN-γ及TNF-α mRNA表达水平均明显升高（P<0.05或P<0.01）,IL-8 mRNA表达水平均明显降低（P<0.05）,Ab-Lac-RV组乳鼠结肠组织中IL-10 mRNA表达水平明显升高（P<0.01）。结论：罗伊氏乳杆菌可能通过上调IL-1β、IL-10、IFN-γ和TNF-α mRNA表达及下调IL-8 mRNA表达，抑制RV复制。

目的：探讨过表达溶质载体家族7成员5 (SLC7A5)基因对大鼠卵巢颗粒细胞凋亡的影响，并阐明其相关机制。方法：4只3周龄SPF级SD雌性大鼠，提取原代大鼠卵巢颗粒细胞，分为阴性对照组（NC组）和促卵泡激素受体（FSHR）染色组（FSHR组）。免疫荧光染色法观察大鼠卵巢颗粒细胞中FSHR蛋白表达情况，鉴定原代大鼠卵巢颗粒细胞是否成功分离。将大鼠卵巢颗粒细胞分为对照组（转染空载体质粒）和OE-SLC7A5组（转染SLC7A5过表达质粒），采用实时荧光定量PCR (RT-qPCR)法和Western blotting法验证细胞转染效率。流式细胞术检测2组卵巢颗粒细胞凋亡率，流式细胞术检测2组不同细胞周期卵巢颗粒细胞百分率，RT-qPCR法检测2组卵巢颗粒细胞中SLC7A5、含半胱氨酸的天冬氨酸蛋白酶（Caspase）-3、Caspase-8和肿瘤坏死因子α (TNF-α) mRNA表达水平，Western blotting法检测2组卵巢颗粒细胞中SLC7A5、Caspase-3、cleaved Caspase-3、Caspase-8、cleaved Caspase-8和TNF-α蛋白表达水平。结果：荧光显微镜下卵巢颗粒细胞呈长梭形或者不规则形，特异性表达FSHR,NC组未见FSHR绿色荧光表达，FSHR组可见FSHR绿色荧光表达，提示大鼠原代卵巢颗粒细胞成功分离。与对照组比较，OE-SLC7A5组卵巢颗粒细胞中SLC7A5 mRNA和蛋白表达水平均明显升高（P<0.05），提示SLC7A5过表达质粒成功转染卵巢颗粒细胞。流式细胞术检测，与对照组比较，OE-SLC7A5组细胞凋亡率明显升高（P<0.05）。与对照组比较，OE-SLC7A5组S期卵巢颗粒细胞百分率明显降低（P<0.05）。RT-qPCR法检测，与对照组比较，OE-SLC7A5组卵巢颗粒细胞中TNF-α、 Caspase-3和Caspase-8 mRNA表达水平均明显升高（P<0.05）。Western blotting法检测，与对照组比较，OE-SLC7A5组卵巢颗粒细胞中TNF-α、Caspase-8、cleaved Caspase-8、Caspase-3、cleaved Caspase-3和SLC7A5蛋白表达水平均明显升高（P<0.05）。结论：SLC7A5蛋白表达增加能够通过上调TNF-α、Caspase-8和Caspase-3凋亡通路表达，促进颗粒细胞凋亡。

目的：探讨姜黄素对人前列腺癌C4-2细胞和LNCaP细胞增殖、迁移及侵袭的影响，并阐明其可能的作用机制。方法：采用慢病毒转染系统分别转染C4-2细胞和LNCaP细胞，作为shCD147-C4-2组和shCD147-LNCaP组。采用RNA干扰技术制备沉默CD147基因细胞，以转入空载体的细胞作为阴性对照，分为shNC-C4-2组（shNC-C4-2细胞）和shNC-LNCaP组（shNC-LNCaP细胞）。取生长对数期C4-2、LNCap、shCD147-C4-2和shCD147-LNCaP细胞，加入20μmol·L^-1姜黄素，处理0和24 h时，显微镜观察各组细胞形态表现。噻唑蓝（MTT）法检测各组细胞增殖活性，细胞划痕实验检测各组细胞迁移率，Western blotting法检测各组细胞中凋亡、侵袭和迁移相关蛋白表达水平。结果：与C4-2组比较，沉默CD147基因后shCD147-C4-2组细胞中CD147蛋白表达量明显减少；与LNCaP组比较，沉默CD147基因后shCD147-LNCaP组细胞中CD147蛋白表达量明显减少。与处理0 h比较，20μmol·L^-1姜黄素处理24 h后C4-2组和LNCaP组部分细胞出现凋亡征象，且有典型凋亡小体存在；shCD147-C4-2组和shCD147-LNCaP组细胞凋亡现象减弱。MTT法检测，与C4-2+0μmol·L^-1姜黄素组比较，C4-2+20μmol·L^-1姜黄素组、C4-2+40μmol·L^-1姜黄素组、C4-2+60μmol·L^-1姜黄素组和C4-2+80μmol·L^-1姜黄素组细胞增殖活性均明显降低（P<0.01）；与LNCaP+0μmol·L^-1姜黄素组比较，LNCaP+20μmol·L^-1姜黄素组、LNCaP+40μmol·L^-1姜黄素组、LNCaP+60μmol·L^-1姜黄素组和LNCaP+80μmol·L^-1姜黄素组细胞增殖活性均明显降低（P<0.01）；与shNC-C4-2组比较，shNC-C4-2+20μmol·L^-1姜黄素组细胞增殖活性明显降低（P<0.01）；与shNC-C4-2+20μmol·L^-1姜黄素组比较，shCD147-C4-2+20μmol·L^-1姜黄素组细胞增殖活性明显升高（P<0.01）；与shNC-LNCaP组比较，shNC-LNCaP+20μmol·L^-1姜黄素组细胞增殖活性明显降低（P<0.01）；与shNC-LNCaP+20μmol·L^-1姜黄素组比较，shCD147-LNCaP+20μmol·L^-1姜黄素组细胞增殖活性明显升高（P<0.01）。细胞划痕愈合实验检测，姜黄素处理24 h，与C4-2组比较，C4-2+20μmol·L^-1姜黄素组和C4-2+40μmol·L^-1姜黄素组细胞迁移率均明显降低（P<0.01）；与LNCaP组比较，LNCaP+20μmol·L^-1姜黄素组和LNCaP+40μmol·L^-1姜黄素组细胞迁移率均明显降低（P<0.01）；与shNC-C4-2组比较，shNC-C4-2+20μmol·L^-1姜黄素组细胞迁移率明显降低（P<0.01）；与shNC-C4-2+20μmol·L^-1姜黄素组比较，shCD147-C4-2+20μmol·L^-1姜黄素组细胞迁移率明显升高（P<0.05）；与shNC-LNCaP组比较，shNC-LNCaP+20μmol·L^-1姜黄素组细胞迁移率明显降低（P<0.01）；与shNC-LNCaP+20μmol·L^-1姜黄素组比较，shCD147-LNCaP+20μmol·L^-1姜黄素组细胞迁移率明显升高（P<0.05）。Western blotting法检测，与C4-2组比较，C4-2+20μmol·L^-1姜黄素组和C4-2+40μmol·L^-1姜黄素组细胞中B细胞淋巴瘤2 （Bcl-2）相关X蛋白（Bax）、裂解的含半胱氨酸的天冬氨酸蛋白酶3 （cleaved Caspase-3）和聚二磷酸腺苷（ADP）-核糖聚合酶1 （PARP1）蛋白表达水平均明显升高（P<0.01）,Bcl-2蛋白表达水平均明显降低（P<0.05或P<0.01）；与LNCaP组比较，LNCaP+20μmol·L^-1姜黄素组和LNCaP+40μmol·L^-1姜黄素组细胞中Bax、cleaved Caspase-3和PARP1蛋白表达水平均明显升高（P<0.01）,LNCaP+40μmol·L^-1姜黄素组Bcl-2蛋白表达水平明显降低（P<0.01）；与shNC-C4-2组比较，shNC-C4-2+20μmol·L^-1姜黄素组细胞中Bax、cleaved Caspase-3和PARP1蛋白表达水平均明显升高（P<0.01）,Bcl-2蛋白表达水平明显降低（P<0.05）；与shNC-C4-2+20μmol·L^-1姜黄素组比较，shCD147-C4-2+20μmol·L^-1姜黄素组细胞中Bax和cleavedCaspase-3蛋白表达水平均明显降低（P<0.01）。与shNC-LNCaP组比较，shNCLNCaP+20μmol·L^-1姜黄素组细胞中Bax、 cleaved Caspase-3和PARP1蛋白表达水平均明显升高（P<0.05或P<0.01）,Bcl-2蛋白表达水平明显降低（P<0.05）；与shNC-LNCaP+20μmol·L^-1姜黄素组比较，shCD147-LNCaP+20μmol·L^-1姜黄素组细胞中Bax、cleaved Caspase-3和PARP1蛋白表达水平均明显降低（P<0.05或P<0.01）,Bcl-2蛋白表达水平明显升高（P<0.05）。与C4-2组比较，C4-2+20μmol·L^-1姜黄素组和C4-2+40μmol·L^-1姜黄素组细胞中E-钙黏蛋白（E-cadherin）蛋白表达水平均明显升高（P<0.01），神经钙黏蛋白（N-cadherin）和波形蛋白（Vimentin）蛋白表达水平均明显降低（P<0.01）；与LNCaP组比较，LNCaP+20μmol·L^-1姜黄素组和LNCaP+40μmol·L^-1姜黄素组细胞中E-cadherin蛋白表达水平均明显升高（P<0.01）,LNCaP+40μmol·L^-1姜黄素组细胞中N-cadherin和Vimentin蛋白表达水平均明显降低（P<0.01）；与shNC-C4-2组比较，shNC-C4-2+20μmol·L^-1姜黄素组细胞中N-cadherin和Vimentin蛋白表达水平均明显降低（P<0.01）；与shNCC4-2+20μmol·L^-1姜黄素组比较，shCD147-C4-2+20μmol·L^-1姜黄素组细胞中E-cadherin蛋白表达水平明显降低（P<0.01）,N-cadherin和Vimentin蛋白表达水平均明显升高（P<0.01）；与shNC-LNCaP组比较，shNC-LNCaP+20μmol·L^-1姜黄素组细胞中E-cadherin蛋白表达水平明显升高（P<0.01）,N-cadherin和Vimentin蛋白表达水平均明显降低（P<0.01）；与shNC-LNCaP+20μmol·L^-1姜黄素组比较，shCD147-LNCaP+20μmol·L^-1姜黄素组细胞中E-cadherin蛋白表达水平明显降低（P<0.01）,N-cadherin表达水平明显升高（P<0.05）。结论：姜黄素对体外前列腺癌细胞增殖、迁移和侵袭有抑制作用，并诱导细胞凋亡，沉默CD147基因可在一定程度上降低其抑制作用和诱导细胞凋亡能力。

牙髓干细胞（DPSCs）是一类具有广泛应用潜力的间充质干细胞。DPSCs因其多向分化潜能和易获取的特点成为眼科领域研究的热点。近年来，DPSCs在角膜上皮损伤和视网膜退行性病变的治疗中表现出潜在的临床应用前景。DPSCs可以通过分化为角膜上皮细胞和抑制M1巨噬细胞，促进角膜上皮再生和重建。此外，DPSCs也可以分化为视网膜光感受器样细胞和视网膜神经节样细胞，替换原有视神经元，分泌神经营养因子介导损伤修复，促进视网膜的再生，改善视网膜原有功能。现系统地回顾近年来国内外相关文献，就DPSCs的生物学特性及其在角膜和视网膜疾病治疗中应用的研究进展进行综述，以期为DPSCs在转化医学和眼科相关疾病治疗中应用的研究提供思路及策略。

Objective To discuss the expression of programmed cell death-ligand 1 （PD-L1） in the oral squamous cell carcinoma （OSCC） cells and its effect on biological behavior of the OSCC CAL27 cells， and to clarify the possible mechanism. Methods Western blotting method was used to detect the expression levels of PD-L1 protein in the oral epithelial HOK cells and OSCC CAL27， TCA8113， and SCC15 cells； immunofluorescence staining method was used to detect the expression and localization of PD-L1 protein in the CAL27 cells. The CAL27 cells were divided into control group （transfected with si-NC） and si-PD-L1 group （transfected with si-PD-L1）. Western blotting method was used to detect the interference efficiency of the cells in two groups； CCK-8 assay was used to detect the proliferative activities of the cells in two groups at different time points； plate clone formation assay was used to detect the numbers of clone formation of the cells in two groups； cell scratch healing assay was used to detect the scratch healing rates of the cells in two groups； Transwell chamber assay was used to detect the numbers of migration and invasion cells in two groups. Results The expression level of PD-L1 protein in the OSCC cells was higher than that in the HOK cells （P<0.05 or P<0.01）； PD-L1 expressed in the cytoplasm and nucleus of the CAL27 cells. The CCK-8 assay and plate clone formation assay results showed that compared with control group， the proliferative activities of the CAL27 cells in si-PD-L1 group at different time points were significantly decreased（P<0.05 or P<0.01）， and the numbers of clone formation were significantly decreased （P<0.01）. The cell scratch healing assay results showed that compared with control group， the scratch healing rates of the cells in si-PD-L1 group were significantly decreased （P<0.05 or P<0.01）. The Transwell chamber assay results showed that compared with control group， the numbers of migration and invasion cells in si-PD-L1 group were significantly decreased （P<0.01）. Conclusion The expression of PD-L1 in the OSCC cells is higher than that in normal oral epithelial cells， and knocking down PD-L1 expression can inhibit the proliferation， clone formation， migration and invasion capabilities of the OSCC cells.

Objective To discuss the effect of prostaglandin E2 （PGE₂）， a pyrogenic mediator， on the discharge activity of warm-sensitive neurons （WSNs） in median preoptic nucleus （MnPO） of hypothalamus in the female mice， and to clarify its mechanism. Methods Coronal brain slices of MnPO were prepared from the female mice. The slices were then perfused with artificial cerebrospinal fluid （ACSF） containing synaptic transmission blockers （STBs）. The discharge frequency was monitored using the patch clamp technique while changing the temperature of the perfusate to identify the WSNs. A total of 32 MnPO WSNs were divided into base line group（n=32） and PEG₂ （n=32）. The patch clamp technique was employed to monitor the discharge frequencies of MnPO WSNs following the perfusion of ACSF and 1 μmol·L^-1 PGE₂， respectively. The MnPO WSNs with good activity and significant change in discharge frequency after PGE₂ perfusion were divided into PGE₂ receptor E-series prostaglandin receptrol （EP）1 antagonist （EP1 ant）+PGE₂ group （n=7）， EP3 ant+PGE₂ group （n=7）， and EP4 ant+PGE₂ group （n=7）. The patch clamp technique was used to monitor the discharge frequencies of MnPO WSNs following the perfusion of 3 μmol·L^-1 EP1 ant and 1 μmol·L^-1 PGE₂ mixture， 10 μmol·L^-1 EP3 ant and 1 μmol·L^-1 PGE₂ mixture， and 10 μmol·L^-1 EP4 ant and 1 μmol·L^-1 PGE₂ mixture， respectively. Resluts： After perfuson of the ACSF containing STBs， a total of 188 MnPO neurons from the female mice with an intrinsic temperature sensitivity coefficient （m value） were identified； out of these， 32 neurons had an m value of ≥0.8 and were identified as MnPO WSNs， accounting for approximately 17% of all recorded neurons. Compared with baseline discharge frequency， the discharge frequency of MnPO WSNs after addition of PGE2 was decreased （P<0.05）. Compared with PGE₂ group， the percentage change in discharge frequency of MnPO WSNs in EP3 ant+PGE₂ group was significantly decreased （P<0.05）. Compared with PGE₂ group， the percentage change in discharge frequency of MnPO WSNs in EP1 ant+PGE₂ group had no significant difference （P>0.05）. Compared with PGE₂ group， the percentage change in discharge frequency of MnPO WSNs in EP4 ant+PGE₂ group had no significant difference（P>0.05）. Conclusion In the female mice， WSNs make up approximately 17% of the total neurons in MnPO. PGE₂ can directly inhibit the discharge activity of MnPO WSNs in the female mice through postsynaptic mechanism involving EP3 receptors.

目的：探讨微小RNA (miR)-30c-5p对人前列腺癌细胞（LNCap）增殖、迁移和侵袭的影响，并阐明其可能的机制。方法：LNCap细胞根据转染质粒不同分为LNCap组（无转染质粒）、miR-30c-5p mimic组（转染miR-30c-5p mimic）、mimic NC组（转染miR-30c-5p mimic NC）、sh-DNA损伤诱导转录因子4 (DDIT4)组（转染sh-DDIT4）、sh-NC组（转染sh-DDIT4 NC）、miR-30c-5p mimic+pc-DNA3.1-NC组（共转染miR-30c-5p mimic和pc DNA3.1-DDIT4空载质粒）和miR-30c-5p mimic+pc-DNA3.1-DDIT4组（共转染miR-30c-5pmimic和pc-DNA3.1-DDIT4过表达质粒），RWPE-1细胞正常培养。实时荧光定量PCR (RT-qPCR)法检测各组细胞中miR-30c-5p和DDIT4mRNA表达水平，Western blotting法检测各组细胞中DDIT4蛋白表达水平，CCK-8法检测各组LNCap细胞增殖率，Transwell小室实验检测各组LNCap细胞侵袭细胞数，划痕实验检测各组LNCap细胞划痕愈合率，双荧光素酶报告基因实验验证miR-30c-5p与DDIT4的靶向关系。体内裸鼠成瘤实验，18只雄性BALB/c裸鼠随机分为空白组、agomiR-NC组（转染agomiR-30c-5p NC）和agomiR-30c-5p组（转染agomiR-30c-5p），每组6只。agomiR-NC组和agomiR-30c-5p组裸鼠皮下注射LNCap细胞，空白组裸鼠注射等量生理盐水，检测各组小鼠肿瘤体积。HE染色观察各组小鼠前列腺癌组织形态表现，RT-qPCR法和免疫荧光染色法检测各组小鼠前列腺癌组织中miR-30c-5p和DDIT4 mRNA表达水平及DDIT4蛋白荧光强度。结果：体外前列腺癌细胞实验，与人正常前列腺上皮RWPE-1细胞比较，前列腺癌LNCap细胞中miR-30c-5p表达水平明显降低（P<0.01）,DDIT4 mRNA和蛋白表达水平明显升高（P<0.05或P<0.01）；转染48 h后，与LNCap组和mimic NC组比较，miR-30c-5p mimic组LNCap细胞中miR-30c-5p表达水平明显升高（P<0.01）。与LNCap组和sh-NC组比较，sh-DDIT4组LNCap细胞中DDIT4 mRNA表达水平明显降低（P<0.01）；与miR-30c-5p mimic组和miR-30c-5p mimic+pcDNA3.1 NC组比较，miR-30c-5p mimic+pc-DNA3.1-DDIT4组LNCap细胞中miR-30c-5p表达水平明显降低（P<0.01）；与miR-30c-5p mimic组和miR-30c-5p mimic+pcDNA3.1 NC组比较，miR-30c-5p mimic+pc-DNA3.1-DDIT4组LNCap细胞中DDIT4 mRNA表达水平明显升高（P<0.01）；与miR-30c-5pmimic组和miR-30c-5pmimic+pcDNA3.1NC组比较，miR-30c-5pmimic+pc-DNA3.1-DDIT4组LNCap细胞中DDIT4蛋白表达水平明显升高（P<0.05）。CCK-8法检测，与LNCap组和mimic NC组比较，miR-30c-5p mimic组LNCap细胞增殖率明显降低（P<0.01）；与LNCap组和sh-NC组比较，sh-DDIT4组LNCap细胞增殖率明显降低（P<0.01）；与miR-30c-5p mimic组和miR-30c-5pmimic+pcDNA3.1NC组比较，miR-30c-5pmimic+pc-DNA3.1-DDIT4组LNCap细胞增殖率明显升高（P<0.01）。Transwell小室实验检测，与LNCap组和mimic NC组比较，miR-30c-5p mimic组LNCap细胞侵袭细胞数明显减少（P<0.01）；与LNCap组和sh-NC组比较，sh-DDIT4组LNCap细胞侵袭细胞数明显减少（P<0.01）；与miR-30c-5pmimic组和miR-30c-5p mimic+pcDNA3.1 NC组比较，miR-30c-5p mimic+pc-DNA3.1-DDIT4组LNCap细胞侵袭细胞数明显增加（P<0.01）。划痕实验检测，与LNCap组和mimic NC组比较，miR-30c-5p mimic组LNCap细胞划痕愈合率明显降低（P<0.01）；与LNCap组和sh-NC组比较，sh-DDIT4组细胞划痕愈合率明显降低（P<0.01）；与miR-30c-5p mimic组和miR-30c-5p mimic+pcDNA3.1 NC组比较，miR-30c-5p mimic+pc-DNA3.1-DDIT4组细胞划痕愈合率明显升高（P<0.01）。双荧光素酶实验检测，与共转染WT-DDIT4和mimic NC的LNCap细胞比较，共转染WT-DDIT4和miR-30c-5p mimic的LNCap细胞中荧光素酶活性明显降低（P<0.01）。体内裸鼠成瘤实验，细胞注射后第3、6、9、12和15天，与空白组和agomiR-NC组比较，agomiR-30c-5p组裸鼠肿瘤体积明显减小（P<0.05）。HE染色观察，空白组和agomiR-NC组小鼠前列腺癌组织中细胞核增大，核仁突出且畸形；agomiR-30c-5p组小鼠前列腺癌组织部分区域细胞排列整齐，细胞核恢复正常形态。RT-qPCR法和免疫荧光染色法检测，与agomiR-NC组比较，agomiR-30c-5p组小鼠前列腺癌组织中miR-30c-5p表达水平明显升高（P<0.01）；与空白组和agomiR-NC组比较，agomiR-30c-5p组小鼠前列腺癌组织中DDIT4 mRNA表达水平明显降低（P<0.01）;DDIT4蛋白主要在细胞质表达，与空白组和agomiR-NC组比较，agomiR-30c-5p组小鼠前列腺癌组织中DDIT4蛋白荧光强度明显降低（P<0.01）。结论：miR-30c-5p在前列腺癌LNCap细胞中表达水平明显降低，其可通过靶向下调DDIT4抑制前列腺癌细胞增殖、迁移和侵袭，从而参与前列腺癌的发生发展。

Objective To discuss the effect of CD40 ligand （CD40L） on the biological behavior of the human monocytic leukemia THP-1 cells through long non-coding RNA（lncRNA） linc00239，and to clarify its potential mechanism. Methods The linc00239 over-expression vector （pcDNA-linc00239） and interference vector （sh-linc00239） were constructed and transfected into the THP-1 cells.Real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the transfection efficiency. The THP-1 cells were divided into control group， vector group， pcDNA-linc00239 group， sh-linc00239 group， vector+CD40L group， pcDNA-linc00239+CD40L group， and sh-linc00239+CD40L group. RT-qPCR method was used to detect the expression levels of linc00239 in the cells in various groups； CCK-8 assay was used to detect the proliferation activities of the cells in various groups；flow cytometry was used to detect the percentages of the cells at different cell cycles and the apoptotic rates of the cells in various groups；RT-qPCR and Western blotting methods were used to to detect the expression levels of B-cell lymphoma-2 （Bcl-2） and Bcl-2-associated X protein （Bax） mRNA and proteins in the cells in various groups； Western blotting method was used to detect the expression levels of protein kinase B （AKT） and phosphorylated AKT （p-AKT） proteins in the cells in various groups，and the ratio of p-AKT/AKT was calculated. Results Compared with vector group， the proliferation activity of the cells and the percentage of the cells at G₂ phase in pcDNA-linc00239 group were significantly increased （P<0.05 or P<0.01）， the expression levels of linc00239， Bcl-2 mRNA and protein， and the ratio of p-AKT/AKT were significantly increased （P<0.05 or P<0.01），the percentage of the cells at G₁ phase， apoptotic rate， and expression levels of Bax mRNA and protein in the cells were significantly decreased （P<0.05）； compared with vector group， the proliferation activity of the cells and percentage of the cells at G₂ phase， expression levels of linc00239， Bcl-2 mRNA and protein， and ratio of p-AKT/AKT in the cells in sh-linc00239 group and vector+CD40L group were significantly decreased （P<0.05 or P<0.01）， while the percentage of the cells at G₁ phase， apoptotic rate， and the expression levels of Bax mRNA and protein in the cells were significantly increased （P<0.05 or P<0.01）；compared with pcDNA-linc00239 group， the proliferation activity of the cells and percentage of cells at G₂ phase in pcDNA-linc00239+CD40L group were significantly decreased （P<0.05 or P<0.01）， the expression levels of linc00239， Bcl-2 mRNA and protein，and ratio of p-AKT/AKT were significantly decreased （P<0.05 or P<0.01），while the percentage of cells at G₁ phase， apoptotic rate， and the expression levels of Bax mRNA and protein were significantly increased （P<0.05 or P<0.01）；compared with sh-linc00239 group， the proliferation activity of the cells and percentage of cells at G₂ phase in sh-linc00239+CD40L group were significantly decreased （P<0.05 or P<0.01）， the expression levels of linc00239， Bcl-2 mRNA and protein， and ratio of p-AKT/AKT were significantly decreased （P<0.05 or P<0.01），and the percentage of the cells at G₁ phase， apoptotic rate， and expression levels of Bax mRNA and protein were significantly increased （P<0.05 or P<0.01）. Conclusion CD40L can inhibit the proliferation and cell cycle progression of the THP-1 cells through linc00239 and induce the apoptosis.

Objective To investigate the efficacy of Balanophora involucrata Hook.f. in treatment of hyperuricemia （HUA） based on network pharmacology， molecular docking， and hyperuricemia models in vivo and in vitro，and to clarify the main targets of its active components and related signaling pathway mechanism. Methods The potential targets of Balanophora involucrata Hook.f. in treatment of HUA were identified by Databases such as the Traditional Chinese Medicine Database in Taiwan， the Chinese Herbal Medicine Identification Database，Professional Chemical Database， TargetNet Database， SwissTargetPrediction Database， GeneCards， Therapeutic Target Database （TTD），DrugBank Database， DisGeNET Database， Online Mendelian Inheritance in Man （OMIM） Database， and Venny Database. STRING Database and Cytoscape software were used to construct the active component-predictive target network and protein-protein interaction （PPI） network for Balanophora involucrata Hook.f.；topological analysis was used to select the main active components and core targets；Gene Ontology （GO） functional and Kyoto Encyclopedia of Genes and Genomes （KEGG） signaling pathway enrichment analysis were performed by R software； AutoDock Vina software was used for molecular docking validation. The NRK-52E cells were divided into blank control group， blank administration group， model group， and different concentrations （2.0， 10.0， and 50.0 μmol·L^-1） of erythrodiol （EDT） groups. High-performance liquid chromatography culture （HPLC） was used to detect the uric acid （UA） levels in the cell culture supernatants in various groups. The male ICR mice were divided into blank control group， blank administration group， model group， and EDT group； the mice in the last two groups were used to prepare the HUA models； kits were used to detect the levels of UA， creatinine （Cr）， and blood urea nitrogen （BUN） in serum of the mice in various groups；the bilateral kidney tissue of the mice was harvested and weighed； the kidney indexes of the mice in various groups were calculated；TUNEL staining was used to observe the apoptosis in kidney tissue of the mice in various groups；Western blotting method was used to detect the expression levels of protein kinase B （AKT），phosphorylated AKT （p-AKT），phosphoinositide 3-kinase （PI3K），phosphorylated PI3K（p-PI3K）， B-cell lymphoma-2 （Bcl-2）， Bcl-2-associated X protein （Bax）， and matrix metalloproteinase-9 （MMP-9） proteins in kidney tissue of the mice in various groups. Results Six active components of Balanophora involucrata Hook.f.were identified， involving 116 intersecting targets and 14 core targets.The enrichment analysis yielded 1 828 GO terms and 145 signaling pathways. The molecular docking results showed that EDT had good binding activity with MMP-9. The high uric acid cell experiment results showed that compared with blank control group， the UA level in the cells in model group was significantly increased （P<0.01）； compared with model group， the UA levels in the cells in 2.0， 10.0， and 50.0 μmol·L^-1 EDT groups were significantly decreased （P<0.01）. Compared with blank control group， the levels of UA， Cr， and BUN in serum of the mice in model group were increased（P<0.01）， and the kidney indexes were significantly increased （P<0.01）； compared with model group， the levels of UA， Cr， and BUN in serum of the mice in EDT group were decreased （P<0.05 or P<0.01），and the kidney index was significantly decreased （P<0.05 or P<0.01）. Compared with blank control group， the number of apoptotic cells in kidney tissue of the mice in model group was increased； compared with model group， the number of the apoptotic cells in kidney tissue of the mice in EDT group was significantly decreased. Compared with blank control group， the ratios of p-AKT/AKT and p-PI3K/PI3K and expression level of Bcl-2 protein in kidney tissue of the mice in model group were significantly decreased （P<0.05 or P<0.01）， while the expression levels of Bax and MMP-9 proteins were significantly increased （P<0.01）； compared with model group， the ratios of p-AKT/AKT and p-PI3K/PI3K and expression level of Bcl-2 protein in kidney tissue of the mice in EDT group were significantly increased （P<0.05 or P<0.01）， and the expression levels of Bax and MMP-9 proteins were significantly decreased （P<0.01）. Conclusion The active component of Balanophora involucrata Hook.f.，EDT，has a UA-decreasing effect and may inhibit the apoptosis and alleviate the kidney injury by activating the PI3K/AKT signaling pathway.

Objective To discuss the differential effects of apolipoprotein E （APOE） gene polymorphism in the neurotoxicity-reactive astrocytes， and to provide the theoretical basis for the study of the pathogenesis of Alzheimer’s disease （AD）. Methods The primary cortical astrocytes from the APOE-knockout mice （APOE ^-/- ） were isolated and cultured in vitro，and the purity of the cells was identified by immunofluorescence staining. The human APOE3 and APOE4 recombinant over-expression plasmids were constructed and separately transfected into the primary APOE ^-/- astrocytes， and the APOE ^-/- primary cells were regarded as control. Western blotting method was used to detect the expression levels of APOE and glial fibrillary acidic protein （GFAP） proteins in the cells； enzyme-linked immunosorbent assay （ELISA） method was used to detect the APOE level in the cellular culture supernatant. The inflammatory models were prepared with the primary astrocytes transfected with APOE3 and APOE4 and co-stimulated with interleukin-1α（IL-1α）， tumor necrosis factor （TNF）， and complement C1q.The cells were divided into APOE3+PBS group， APOE4+PBS group， APOE3+IL-1α+TNF+C1q group， and APOE4+IL-1α+TNF+C1q group. Cell immunofluorescence staining method was used to observe the morphology of the cells in various groups； real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the expression levels of glypican 4 （Gpc4）， glypican 6 （Gpc6）， thrombospondin 1 （Thbs1）， thrombospondin 2 （Thbs2）， SPARC-like protein 1 （Sparcl1） and glial cell line derived neurotrophic factor （GDNF）， C3，and S100 calcium binding protein B （S100B） mRNA in the cells in various groups； microsphere phagocytosis assay was used to detect the phagocytic capacities of the cells in various groups； Western blotting was used to detect the protein expression levels of B-cell lymphoma 2 （Bcl-2），and cysteinyl aspartate specific protease-3 （Caspase-3） proteins in the cells in various groups. Results Compared with APOE ^-/- group， the expression levels of APOE and GFAP proteins in the cells and the APOE level in the cellular culture supernatant in transfected APOE3 and transfected APOE4 groups were increased （P<0.01）. The fluorescence microscope observation results showed that compared with APOE3+PBS and APOE4+PBS groups， the astrocytic processes in APOE3+IL-1α+TNF+Cq1 group and APOE4+IL-1α+TNF+Cq1 group became shorter and the cell bodies became larger； compared with APOE3+IL-1α+TNF+Cq1 group， the astrocytic processes in APOE4+IL-1α+TNF+Cq1 group were even shorter. Compared with APOE3+PBS and APOE4+PBS groups， the expression levels of Gpc4， Gpc6， Thbs1， Thbs2，and Sparcl1 mRNA in the cells in APOE3+IL-1α+TNF+Cq1 group and APOE4+IL-1α+TNF+Cq1 group were significantly decreased （P<0.01）； compared with APOE3+IL-1α+TNF+Cq1 group， the expression levels of Gpc4， Gpc6，Thbs1， Thbs2， and Sparcl1 mRNA in the cells in APOE4+IL-1α+TNF+Cq1 group were significantly decreased （P<0.05 or P<0.01）. Compared with APOE3+PBS and APOE4+PBS groups， the expression levels of GDNF mRNA in the cells in APOE3+IL-1α+TNF+Cq1 group and APOE4+IL-1α+TNF+Cq1 group were decreased（P<0.01），and the expression levels of C3 and S100B mRNA were increased（P<0.01）；compared with APOE3+IL-1α+TNF+Cq1 group， the expression level of GDNF mRNA in the cells in APOE4+IL-1α+TNF+Cq1 group was decreased（P<0.05），and the expression levels of C3 and S100B mRNA were increased（P<0.05）. Compared with APOE3+PBS group and APOE4+PBS group，the numbers of hagocytosis of microspheres in the cells in APOE3+IL-1α+TNF+Cq1 group and APOE4+IL-1α+TNF+Cq1 group were significantly decreased； compared with APOE3+IL-1α+TNF+Cq1 group，the number of hagocytosis of microspheres in the cells in APOE4+IL-1α+TNF+Cq1 group was significantly decreased. Compared with APOE3+PBS group and APOE4+PBS group，the expression levels of Bcl-2 protein in the cells in APOE3+IL-1α+TNF+Cq1 group and APOE4+IL-1α+TNF+Cq1 group were decreased （P<0.05 or P<0.01）and the expression levels of Caspase-3 protein were significantly increased（P<0.01）；compared with APOE3+IL-1α+TNF+Cq1 group， the expression level of Bcl-2 protein in the cells in APOE4+IL-1α+TNF+Cq1 group was decreased（P<0.01），and the expression level of Caspase-3 protein was increased（P<0.05）. Conclusion The APOE4 genotype has a stronger ability to induce the inflammatory factors compared with APOE3；it can lead to a neurotoxicity-reactive astrocyte phenotype，increase the neurotoxicity，affect the astrocyte apoptosis， and aggravate the neuron damage.

Objective To discuss the inhibitory effect of chelerythrine （CHE） on the migration， invasion， and epithelial-mesenchymal transition （EMT） of the human ovarian cancer SKOV3 cells，and to clarify the associated mechanism. Methods The SKOV3 cells were cultured in vitro and divided into control group and 2.5， 5.0， 10.0， 20.0， and 40.0 μmol·L^－1 CHE groups.Methylthiazolydiphenyl-tetrazolium（MTT） assay was used to detect the inhibitory rates of proliferation of the cells in various groups. The SKOV3 cells were cultured in vitro and divided into control group， transforming growth factor-β1 （TGF-β1） group， TGF-β1+5 μmol·L^－1 CHE group， and TGF-β1+10 μmol·L^－1 CHE group.Cell scratch assay was used to detect the migration rates of the cells in various groups； Transwell chamber assay was used to detect the numbers of migration and invasion cells in various groups； Western blotting method was used to detect the expression levels of E-cadherin， N-cadherin， and Vimentin proteins in the cells in various groups； immunofluorescence staining method was used to detect the fluorescence intensities of E-cadherin and N-cadherin in the cells in various groups. Results The MTT assay results showed that compared with control group， the inhibitory rates of proliferation of the cells in 5.0， 10.0， 20.0， and 40.0 μmol·L^－1 CHE groups were significantly increased （P<0.05 or P<0.01）. The cell scratch assay results showed that compared with control group， the migration rate of the cells in TGF-β1 group was increased （P<0.01）； compared with TGF-β1 group， the migration rates of the cells in TGF-β1+5 μmol·L^－1 CHE group and TGF-β1+10 μmol·L^－1 CHE group were significantly decreased （P<0.01）. The Transwell chamber assay results showed that compared with control group， the numbers of migration and invasion cells in TGF-β1 group were significantly increased （P<0.05）； compared with TGF-β1 group， the numbers of migration and invasion cells in TGF-β1+5 μmol·L^－1 CHE group and TGF-β1+10 μmol·L^－1 CHE group were significantly decreased （P<0.01）. The Western blotting results showed that compared with control group， the expression level of E-cadherin protein in the cells in TGF-β1 group was significantly decreased （P<0.01）， while the expression levels of N-cadherin and Vimentin proteins were increased （P<0.05 or P<0.01）； compared with TGF-β1 group， the expression levels of E-cadherin protein in the cells in TGF-β1+5 μmol·L^－1 CHE group and TGF-β1+10 μmol·L^－1 CHE group were significantly increased （P<0.01）， and the expression levels of N-cadherin and Vimentin proteins were significantly decreased （P<0.01）. The immunofluorescence staining results showed that compared with control group， the fluorescence intensity of E-cadherin in the cells in TGF-β1 group was decreased， and the fluorescence intensity of N-cadherin was increased； compared with TGF-β1 group， the fluorescence intensities of E-cadherin in the cells in TGF-β1+5 μmol·L^－1 CHE group and TGF-β1+10 μmol·L^－1 CHE group were significantly increased， and the fluorescence intensities of N-cadherin were decreased. Conclusion CHE can inhibit the proliferation， migration， invasion， and EMT of the human ovarian cancer SKOV3 cells.

目的：探讨白藜芦醇对颞下颌关节骨关节炎（TMJOA）的治疗作用，并阐明相关作用机制。方法：45只SD大鼠随机分为对照组、模型组和白藜芦醇组，每组15只。模型组和白藜芦醇组大鼠关节腔内注射20 g·L-1碘乙酸钠（MIA） 50μL，构建TMJOA大鼠模型；对照组大鼠注射等量生理盐水。造模3周后，白藜芦醇组大鼠注射80μL白藜芦醇溶液，每周1次，连续3周，对照组和模型组大鼠注射等量生理盐水。微型计算机断层扫描技术（Micro-CT）系统检测各组大鼠髁突结构，计算感兴趣区的骨体积分数（BV/TV）、骨小梁厚度（Tb. Th）、骨小梁间距（Tb. p）和骨小梁数（Tb. N）。HE染色和甲苯胺蓝染色观察各组大鼠颞下颌关节（TMJ）组织病理形态表现，免疫组织化学法检测各组大鼠TMJ组织中性别决定区Y框蛋白（SOX）-9、基质金属蛋白酶（MMP）-13、沉默信息调节因子（Sirt）1、磷脂酰肌醇3激酶（PI3K）、磷酸化蛋白激酶B (p-Akt)和磷酸化哺乳动物雷帕霉素靶蛋白（p-mTOR）蛋白表达水平，实时荧光定量PCR (RT-qPCR)法检测各组大鼠TMJ组织中SOX-9、MMP-13、Sirt1、PI3K、哺乳动物雷帕霉素靶蛋白（mTOR）和蛋白激酶B (Akt) mRNA表达水平。结果：造模3周后，大鼠髁突骨质破坏明显，表面粗糙不平，延续性中断，表明TMJOA大鼠模型造模成功。Micro-CT系统检测，对照组大鼠髁突表面光滑，形态规则，骨质连续完整；模型组大鼠髁突破坏明显，骨质连续性受到不同程度破坏，表面粗糙可伴有不同程度骨质缺损；白藜芦醇组大鼠髁突病变减轻，髁突形态外观得到一定的改善。与对照组比较，模型组大鼠BV/TV和Tb. Th均明显降低（P<0.05）,Tb. Sp明显增加（P<0.05）；与模型组比较，白藜芦醇组大鼠BV/TV和Tb. Th均明显升高（P<0.05）,Tb. Sp明显减少（P<0.05）。HE染色观察，对照组大鼠髁突层次清晰，软骨细胞排列规则，整齐有序；模型组大鼠髁突表面粗糙不平，缺损明显，呈现典型的TMJOA表现；白藜芦醇组大鼠髁突表面略微粗糙，整体分层大致清晰，细胞排列较为有序。甲苯胺蓝染色观察，对照组大鼠髁突肥大层软骨细胞呈蓝紫色，染色明显且均匀；模型组大鼠髁突肥大层软骨细胞淡染，部分区域甚至失染；白藜芦醇组大鼠髁突肥大细胞层染色基本明显且较为均匀。免疫组织化学法检测，与对照组比较，模型组大鼠TMJ组织中MMP-13、PI3K、p-Akt和p-mTOR蛋白表达水平均明显升高（P<0.05）,SOX-9和Sirt1蛋白表达水平均明显降低（P<0.05）；与模型组比较，白藜芦醇组大鼠TMJ组织中SOX-9和Sirt1蛋白表达水平均明显升高（P<0.05）,MMP-13、PI3K、p-Akt和p-mTOR蛋白表达水平均明显降低（P<0.05）。RT-qPCR法检测，与对照组比较，模型组大鼠TMJ组织中MMP-13、PI3K、Akt和mTOR mRNA表达水平均明显升高（P<0.05）,SOX-9和Sirt1 mRNA表达水平均明显降低（P<0.05）；与模型组比较，白藜芦醇组大鼠TMJ组织中SOX-9和Sirt1 mRNA表达水平均明显升高（P<0.05）,MMP-13、PI3K、Akt和mTOR mRNA表达水平均明显降低（P<0.05）。结论：白藜芦醇对TMJOA有治疗作用，其作用机制可能是通过激活Sirt1、抑制PI3K-Akt-mTOR信号通路实现的。

脂蛋白a [Lp (a)]是由载脂蛋白A (apo A)、apo B100和胆固醇酯核心共同组成的高度多态性脂蛋白分子；钙化性主动脉瓣狭窄（CAVS）是由环境和遗传因素共同参与的多因素心脏瓣膜病，Lp (a)是CAVS发病的独立危险因素，可增加CAVS的发病风险。Lp (a)在CAVS的治疗过程中发挥重要作用，尽管目前临床上仍以手术作为CAVS的主要治疗手段，但随着对其病理机制的深入探索，以Lp (a)为潜在治疗靶点的药物治疗也成为一种新的方法。现就Lp (a)的结构、特点及其在CAVS发生发展中的作用、高脂蛋白a血症相关治疗和通过抵抗炎症对CAVS进行预防及治疗的研究进行综述，提高临床医生对高脂蛋白a血症的了解和重视，为CAVS的预防及靶向药物治疗提供新的思路。

目的：分析1例腹股沟精原细胞瘤睾丸精原细胞瘤患者的临床资料，为该类患者诊断和治疗提供参考。方法：收集1例原发性腹股沟精原细胞瘤患者的临床症状、影像学特征、病理学表现和诊断及治疗方法，并进行文献复习。结果：患者，男性，43岁，因偶然发现左侧腹股沟肿物入院，专科查体肿块、边界尚清，表面欠光整，可触及结节和局部波动感，活动欠佳，无表皮溃疡，肤温略高，双侧睾丸形态和大小正常且无压痛。辅助检查，甲胎蛋白（AFP） 2.3 mg·L^-1、β-绒毛膜促性腺激素（HCG）<0.1 IU·L^-1、乳酸脱氢酶（LDH） 254.31 IU·L^-1，肝功、肾功、血常规和凝血常规均正常，胸部CT、心电图、心脏彩超、肝胆脾胰彩超和后腹膜彩超均未见异常。肿瘤科术前穿刺病理结果提示精原细胞瘤，经临床综合分析后决定行腹股沟肿物切除术和腹股沟淋巴结清扫术，术后病理与术前病理结果一致，均为精原细胞瘤且伴腹股沟淋巴结转移，术后1、3、6和8个月随访，患者恢复良好，无任何不适，能从事轻度体力活动，且病情稳定，无进展表现，目前已于肿瘤科行3次放化疗。结论：原发性腹股沟精原细胞瘤治愈率高，恶性度普遍较低，对放疗和化疗敏感，预后良好。

目的：探讨嗜酸性粒细胞（EOS）在宫颈组织中的浸润差异及其与宫颈相关疾病之间的关系，阐明EOS对宫颈上皮不典型增生（CIN）和宫颈癌发生发展的影响。方法：收集256例宫颈疾病患者的临床资料，根据其发病情况分为宫颈癌组（n=46，其中宫颈鳞状细胞癌26例、宫颈腺癌15例和宫颈腺鳞癌5例）、慢性宫颈炎组（n=50）、CINⅠ期组（n=50）、CINⅡ期组（n=50）、CINⅢ期组（n=30）和正常组（癌旁正常宫颈组织，n=30）。阴道镜观察各组患者宫颈组织形态表现，薄层液基细胞学测试（TCT）法观察各组患者宫颈脱落细胞形态表现，杂交捕获-化学发光法检测各组患者宫颈组织人乳头瘤病毒（HPV）感染情况，HE染色观察各组患者宫颈组织病理形态表现，刚果红染色检测各组患者宫颈组织中EOS浸润数，Pearson相关性分析EOS浸润数与宫颈癌恶性程度的相关性。结果：正常组患者宫颈表面光滑，呈粉红色，毛细血管均匀分布；慢性宫颈炎组患者宫颈表面呈红色炎性改变，部分伴有纳氏囊肿形成，可见不同程度的糜烂和溃疡等；CINⅠ期、CINⅡ期和CINⅢ期组患者宫颈可见上皮溃疡、增厚和形态不规则，细镶嵌及点状血管明显；宫颈癌组患者宫颈表面隆起，可见新生肿物及坏死性溃疡，质脆易出血。醋酸染色后，正常组患者宫颈无明显改变；慢性宫颈炎组患者宫颈呈少量白色改变，持续时间较短；CINⅠ期、CINⅡ期和CINⅢ期组患者宫颈薄醋白上皮不规则、呈地图样边界，其中CINⅠ期组患者宫颈部分组织呈醋白反应，CINⅡ期组患者宫颈出现明显醋白反应，CINⅢ期组患者宫颈醋白反应非常明显，面积较大，且持续时间较长；宫颈癌组患者宫颈醋白反应明显，白色上皮厚，持续时间久，轮廓硬直，边界清晰。正常组患者宫颈碘染色后呈棕褐色，着色均匀；慢性宫颈炎组患者宫颈炎性病变区着色差；CINⅠ期组患者宫颈上皮化生区碘着色不明显；CINⅢ期组患者宫颈病变区着色差，转化区周围面积较大；宫颈癌组患者宫颈表面不规则，呈菜花样生长，碘染色后不着色，呈现为橘黄或芥末黄色。TCT法观察，正常组患者宫颈脱落细胞中无异型性细胞，炎症细胞浸润少；慢性宫颈炎组患者宫颈脱落细胞中可见大量的中性粒细胞和EOS等炎症细胞，无异型性细胞；CINⅠ期和CINⅡ期组患者宫颈脱落细胞中可见双核异型性细胞，核质比较高，细胞核较深染，周围见空晕；CINⅢ期组患者脱落细胞中可见较多异型性细胞，核质比较高，核膜不规则；宫颈癌组患者宫颈脱落细胞中可见大而显著的核仁，聚集成片，合胞体样改变明显；与正常组比较，CINⅠ期组、CINⅡ期组、CINⅢ期组和宫颈癌组患者宫颈脱落细胞异型性均明显增加。杂交捕获-化学发光法检测，与正常组和慢性宫颈炎组比较，CINⅠ期、CINⅡ期和CINⅢ期组患者HPV感染数和TCT异型性细胞数均明显增加（P<0.05）；与CINⅠ期、CINⅡ期和CINⅢ期组比较，宫颈癌组患者HPV感染数和TCT异型性细胞数均明显增加（P<0.05）。HE染色观察，正常组宫颈组织细胞形态正常，结构清晰，可见中性粒细胞、单核细胞、巨噬细胞、EOS和淋巴细胞等炎症细胞浸润；慢性宫颈炎组患者炎症细胞浸润增加；CIN组患者宫颈细胞核核仁稍大，可见异型性细胞，炎症细胞主要分布于异型性细胞周围；宫颈癌组患者宫颈细胞核仁大而深染，细胞异型性明显，癌细胞周围炎症细胞浸润增加。与正常组比较，慢性宫颈炎组患者宫颈组织中炎症细胞数和EOS浸润数均明显增加（P<0.05）,CIN组患者炎症细胞数和EOS浸润数均明显增加（P<0.05）；与慢性宫颈炎组比较，CIN组患者炎症细胞数和EOS浸润数均明显减少（P<0.05）；与慢性宫颈炎组和CIN组比较，宫颈癌组患者炎症细胞数和EOS浸润数均明显增加（P<0.05）。宫颈癌组织中EOS主要分布于癌巢周围，与CINⅠ期组比较，CINⅡ期组和CINⅢ期组患者宫颈组织中EOS浸润数均明显增加（P<0.05）；与CINⅡ期组比较，CINⅢ期组患者宫颈组织中EOS浸润数明显增加（P<0.05）。肿瘤恶性程度越高，EOS浸润越多，EOS浸润数与宫颈癌浸润深度呈正相关关系（r=0.533 0,P<0.01）。结论：HPV感染和EOS浸润具有促进宫颈癌癌前病变及宫颈癌发生发展的作用。

目的：评价司库奇尤单抗治疗成人中重度斑块状银屑病的临床疗效和安全性。方法：收集183例接受司库奇尤单抗治疗的成人中重度斑块状银屑病患者的临床资料，第0、1、2、3和4周每周皮下注射司库奇尤单抗1次，其后每4周注射1次，每次300 mg，随访52周。计算银屑病患者的银屑病面积及严重指数（PASI）、体表受累面积（BSA）、基线研究者整体评估（IGA）及平均皮肤病生活质量指数（DLQI）评分，以银屑病患者是否达到PASI 100，分为痊愈组和非痊愈组，评价司库奇尤单抗治疗中重度斑块状银屑病的临床疗效和安全性，并分析其影响因素。结果：与治疗0周时比较，司库奇尤单抗治疗第4、12、24和52周患者PASI、BAS、IGA及DLQI评分均明显降低（P<0.05）。司库奇尤单抗治疗后PASI 75、PASI 90和PASI 100患者百分率于第4周分别为95.6%、84.2%和47.5%，第12周分别为97.3%、95.6%和78.7%，第24周分别为97.8%、96.7%和84.2%，第52周分别为98.4%、 97.8%和83.6%; BSA≤1%患者百分率于第4、 12、 24和52周分别为80.9%、94.5%、95.6%及94.0%;IGA 0/1患者百分率于第4、12、24和52周分别为86.3%、97.3%、96.7%及95.6%;DLQI 0/1患者百分率于第4、12、24和52周分别为76.6%、89.1%、92.9%及91.8%。司库奇尤单抗治疗第4周，2组患者年龄、体质量指数（BMI）、病程、基线PASI评分和既往生物制剂治疗史患者百分率比较差异均有统计学意义（P<0.05）；司库奇尤单抗治疗第24周，2组患者年龄和BMI比较差异有统计学意义（P<0.05）。司库奇尤单抗治疗第4周，BMI≥25 kg·m^-2、病程≥10年、基线PASI评分≥10和有既往生物制剂治疗史是影响患者痊愈的危险因素（P<0.05）；司库奇尤单抗治疗第24周，年龄≥40岁是影响患者痊愈的危险因素（P<0.05）。183例银屑病患者在治疗期间共44例患者报告49次不良反应，出现不良反应患者百分率为24.0%，无严重不良事件和致死性不良反应发生。不良反应包括上呼吸道感染23例、湿疹样皮损10例、皮肤真菌感染6例、荨麻疹3例、肝功能轻度异常2例、毛囊炎2例、结膜炎2例和中耳炎1例。结论：司库奇尤单抗治疗成人中重度斑块状银屑病起效迅速且疗效持久，BMI、病程、基线PASI评分、既往生物制剂治疗史和年龄是司库奇尤单抗临床疗效的影响因素，其总体安全性良好，可作为中重度斑块状银屑病的一线治疗药物。

目的：探讨敲低受体相互作用蛋白激酶3 （RIP3）对缺氧复氧（H/R）诱导下人肾小管上皮HK2细胞自噬、焦亡和铁死亡的影响。方法：将慢病毒干扰载体质粒shRIP3和阴性对照慢病毒干扰载体质粒shNC分别转染至HK2细胞中，分为shRIP3组和shNC组，另以正常培养未转染的HK2细胞作为空白组，转染48 h后，采用实时荧光定量PCR （RT-qPCR）法和Western blotting法验证慢病毒转染效果。将HK2细胞分为对照组、H/R组、shNC+H/R组和shRIP3+H/R组。CCK-8法检测各组HK2细胞存活率，免疫荧光染色法检测各组细胞中微管结合蛋白1轻链（LC） 3B和含核苷酸结合结构域富亮氨酸重复序列（NLR）家族Pyrin域蛋白3 （NLRP3）蛋白荧光强度，Western blotting法检测各组HK2细胞中LC3Ⅱ、LC3Ⅰ、Beclin1、含半胱氨酸的天冬氨酸蛋白酶（Caspase）-1、膜穿孔蛋白D （GSDMD）、白细胞介素（IL）-1β和IL-18蛋白表达水平，试剂盒检测各组细胞中铁离子(Fe²⁺)水平。结果：与空白组和shNC组比较，shRIP3组HK2细胞中RIP3 mRNA和蛋白表达水平均明显降低（P<0.05）。CCK-8法检测，与对照组比较，H/R组HK2细胞存活率明显降低（P<0.05）；与H/R组比较，shRIP3+H/R组HK2细胞存活率明显升高（P<0.05）。免疫荧光染色法检测，与对照组比较，H/R组HK2细胞中LC3B蛋白荧光强度明显降低（P<0.05）,NLRP3蛋白荧光强度明显升高（P<0.05）；与H/R组比较，shRIP3+H/R组HK2细胞中LC3B蛋白荧光强度明显升高（P<0.05）,NLRP3蛋白荧光强度明显降低（P<0.05）。Western blotting法检测，与对照组比较，H/R组HK2细胞中LC3Ⅱ/LC3Ⅰ比值明显降低（P<0.05）,Beclin1蛋白表达水平明显降低（P<0.05）；与H/R组比较，shRIP3+H/R组HK2细胞中LC3Ⅱ/LC3Ⅰ比值明显升高（P<0.05）,Beclin1蛋白表达水平明显升高（P<0.05）；与对照组比较，H/R组HK2细胞中Caspase-1、GSDMD、IL-1β和IL-18蛋白表达水平均明显升高（P<0.05）；与H/R组比较，shRIP3+H/R组HK2细胞中Caspase-1、GSDMD、IL-1β和IL-18蛋白表达水平均明显降低（P<0.05）。与对照组比较，H/R组HK2细胞中GPX4和SLC7A11蛋白表达水平均明显降低（P<0.05）；与H/R组比较，shRIP3+H/R组HK2细胞中GPX4和SLC7A11蛋白表达水平均明显升高（P<0.05）。与对照组比较，H/R组HK2中细胞Fe²⁺水平明显升高（P<0.05）；与H/R组比较，shRIP3+H/R组HK2细胞中Fe²⁺水平明显降低（P<0.05）。结论：靶向敲低RIP3可诱导H/R诱导人肾小管上皮HK2细胞自噬，抑制细胞焦亡和减轻铁死亡。

Gag-Pol protein is one of the important structural proteins of human immunodeficiency virus （HIV）， comprising the basic scaffold proteins and functional enzymes required during the lifecycle of HIV. Currently，the inhibitors targeting different functional domains on Gag-Pol include capsid（CA） inhibitors，protease inhibitors， reverse transcriptase inhibitors， and integrase inhibitors. The CA inhibitors inhibit the maturation of CA or disrupt the assembly of CA，so as to affect the replication of HIV. The primary mechanism of protease inhibitors is to inhibit the protease from cleaving at the cleavage site CA-spacer peptide 1（SP1）. The reverse transcriptase inhibitors block the reverse transcription process of HIV by mimicking the reverse transcription substrates. The integrase inhibitors impact the activity of integrase by targeting the zinc-finger structure at the active center of integrase. This article summarizes the inhibitors targeting HIV Gag-Pol protein and their mechanisms， and reviews the approved dosages and usages of approved patent drugs，so as to provide the references for the future clinical combination therapies and the development of new inhibitors targeting HIV Gag-Pol protein.

Objective To discuss the clinical presentations， diagnosis， and treatment methods of the patients with Fournier’s gangrene， and to enhance the clinicians’ awareness of this condition. Methods The clinical data including symptoms， signs， radiological findings， and surgical outcomes of one patient with Fournier’s gangrene were collected.The relevant literatures were reviewed to summarize the clinical characteristics， diagnosis， and treatment methods for this condition. Results The patient， a 42-year-old male， was admitted because of a history of infection around the perineum， scrotum， and perianal area for 13 d. His medical history included acute myeloid leukemia for 10 months， during which the patient underwent eight chemotherapy sessions in the local hospital. The abdominal CT scan results showed thickened， dense， and turbid soft tissue in the left inguinal area. The complete blood count reuslts showed the white blood cell count was 23.99×10⁹ L^-1. The cultures of wound secretions grew the Escherichiacoli and Proteus mirabilis. The examination results showed there was necrosis of the scrotal skin and skin near the anus on the left buttock； the skin was blackened， hard， and demarcated from the surrounding normal skin with slight purulent exudation and no foul smell. The surrounding skin was significantly swollen and red； the rectal examination results showed no bleeding or fistulas. The patient underwent emergency debridement surgery on the admission day， followed by dressing changes， multiple applications of simplified negative pressure， perineal flap reconstruction， and skin grafting. The patient recovered well with normal function and had no complications. Conclusion Fournier gangrene has acute onset and rapid progression， and the clinical manifestations are non-specific. The range of infection is not consistent with the progression of the disease. The diagnosis mainly depends on intraoperative exploration. Repeated radical surgery is the main treatment. The prognosis of this disease is good， and the recurrence rate is low， although long-term follow-up is still necessary after surgery.

Objective To analyze the clinical data of the patients with leucine-rich glioma inactivated 1 （LGI-1） antibody-positive autoimmune encephalitis （AE） （LGI-1 AE） complicated with sleep structure abnormality and cognitive impairment， and to discuss the possible pathogenic mechanism. Methods A 68-year-old male patient was admitted to our hospital due to memory decline for 2 months and seizures for 1 month.After diagnosed with LGI-1 AE， the patient was treated with intravenous immunoglobulin combined with methylprednisolone sodium succinate， resulting in the improved symptoms. Excluding any pharmaceutical influences， the neuropsychological assessments， including sleep evaluations with polysomnography （PSG）， were performed during both the acute phase and the recovery phase. Results During the acute phase assessment， the patient exhibited severe cognitive impairments， scoring 22 on the Mini-Mental State Examination （MMSE） and 19 on the Montreal Cognitive Assessment （MoCA）.The PSG results showed that the total sleep time （265 min） was shortened， the sleep fragmentation throughout could be seen， the sleep efficiency was reduced， and N3 and rapid eye movement （REM） sleep stages were complete absent. In the recovery phase， the patient’s cognitive functions improved （MMSE score was 30， MoCA score was 26）， the total sleep time returned to normal with PSG， the sleep onset latency was 13.5 min， the sleep fragmentation notably improved， the sleep efficiency was increased to 84.3%，the N3 sleep lasted 26 min （5.1%）， and the REM sleep lasted 69 min （13.6%）. Conclusion The abnormality in sleep structure and cognitive impairment in the patients with LGI-1 AE are synchronous in onset and outcome， and may be one of the etiologies of cognitive dysfunction in these patients. The pathological origin of the sleep disorder may lie in the hypothalamus. Hypothalamic secretions and the Lhx6 pathway might become new targets for correcting the sleep structure while treating the cognitive impairment.

Objective To analyze the intraoperative hemodynamic management by hypotension prediction index （HPI） in one patient underwent robot-assisted laparoscopic cystectomy， and to provide the reference for anesthesia monitoring and hemodynamic management in the similar major surgery. Methods The clinical data， intraoperative hemodynamic data， usage and dosage of vasoactive drugs， and clinical outcomes of one patient underwent robot-assisted laparoscopic cystectomy with HPI-guided intraoperative hemodynamic management were retrospectively analyzed， and the relevant literatures were reviewed. Results The patient， a 72-year-old female， was admitted due to macroscopic hematuria for 5 months accompanied by dysuria for 3 months. The cystoscope results showed a 7 cm×7 cm×5 cm mass on the right side of the bladder trigone and a 4 cm×3 cm×3 cm mass near the bladder neck. The positron emission tomography/computed tomography （PET/CT） results showed thickening of the right posterior bladder wall with high metabolism， and the preliminary diagnosis was bladder malignancy. After preoperative anesthesia evaluation， the robot-assisted laparoscopic cystectomy was planned. After entering the operating room， the routine monitoring was conducted， and the monitor equipped with HPI software was used to guide intraoperative hemodynamic management. After routine anesthesia induction， the tracheal intubation was performed by video laryngoscope. The patient experienced intraoperative hypotension （IOH） for six times， the cumulative time of mean arterial pressure （MAP）<65 mmHg was 13.7 min， accounting for 4.40% of the anesthesia duration， and the time-weighted average of MAP<65 mmHg was 0.28 mmHg. The time range with HPI≥85 roughly overlapped with and included the period of MAP<65 mmHg. At 146 time points with HPI≥85，the MAP remained greater than 65 mmHg at 68.5% （100/146） of the points. At 47 time points with MAP<65 mmHg， HPI≥85 occurred at 97.9% （46/47） of the points. On the first postoperative day， the patient’s hypersensitive cardiac troponin I was <0.01 μg·L^-1， and no perioperative adverse events occurred. The patient was discharged on the eighth day. Conclusion HPI can promptly and accurately predict the occurrence of IOH in the patients undergoing robot-assisted laparoscopic cystectomy. The use of HPI-based hypotension correction strategies during surgery can maintain the time-weighted average of MAP<65 mmHg at a lower level.

Objective To study the expression levels of long non-coding RNA （lncRNA） H19 and insulin-like growth factor 2 （IGF2） genes in breast cancer tissue， and to analyze their imprinting status. Methods Real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the expression levels of H19 and IGF2 mRNA in breast cancer tissue and adjacent tissue， and the differences in the expressions of H19 and IGF2 mRNA in breast cancer tissue and adjacent tissue were analyzed； single nucleotide polymorphism （SNP） was used to distinguish the allele expression status （homozygous or heterozygous）. For heterozygous IGF2 （ApaⅠ site） or H19 （AluⅠ site） in genomic DNA， imprinting analysis was used to detect the imprinting status of H19 and IGF2 in breast cancer tissue， that were maintenance of imprinting （MOI） or loss of imprinting （LOI）； the relationship between the expressions of H19 and IGF2 and molecular subtypes in breast cancer tissue were also analyzed. Results The RT-qPCR results showed that the expression levels of H19 and IGF2 mRNA in breast cancer tissue were higher than those in adjacent tissue （P<0.01）. There was a positive correlation between the expression levels of H19 mRNA and IGF2 mRNA （r=0.567， P<0.01）. Compared with adjacent tissue， the expression levels of H19 mRNA in cancer tissue of the breast cancer patients with various molecular subtypes were increased （P<0.05 or P<0.01）. LOI was observed in both H19 and IGF2 in breast cancer tissue， and the incidence of IGF2 LOI was 36.7%， which was higher than that of H19 LOI（4.3%）. The RT-qPCR results showed that the expression level of IGF2 mRNA in breast cancer tissue in IGF2 LOI group was significantly higher than that in IGF2 MOI group （P<0.01）. Conclusion The expression levels of H19 and IGF2 mRNA in breast cancer tissue are significantly higher than those in adjacent tissue. The incidence of IGF2 LOI is higher than that of H19 LOI， and IGF2 LOI may be one of the key factors in the pathogenesis of breast cancer.

Objective To analyze gene expression data of esophageal adenocarcinoma （EAC） in the Gene Expression Omnibus （GEO） and The Cancer Genome Atlas （TCGA） databases and clarify the relationship between the potential core genes and tumor lymphocyte infiltration in the EAC， and to provide the molecular targets for the diagnosis and treatment of EAC. Methods The high-throughput chip datasets GSE13898， GSE26886， GSE74553， and GSE92396， including EAC and normal esophageal tissues， were downloaded from the GEO database by searching for “esophageal adenocarcinoma”. The limma package of R software was used to screen the differentially expressed genes （DEGs） in EAC tissue and esophageal normal tissue， and the common DEGs were obtained through Venn diagram. After the DEGs were analyzed by STRING database， the results were imported into Cytoscape software to screen the core genes and construct the protein-protein interaction （PPI） network. The Gene Expression Profiling Interactive Analysis （GEPIA） database was used to verify the expression levels of core genes. The UALCAN and Kaplan-Meier Plotter databases were used to analyze the correlations between the core genes and prognosis and clinical data of the EAC patients. The Tumor Immune Estimation Resource （TIMER） database was used to analyze the relationship between core genes and tumor immune infiltration. Gene Ontology （GO） functional and Kyoto Encyclopedia of Genes and Genomes （KEGG） signaling pathway enrichment analysis were performed to analyze the positively correlated genes of core genes obtained from the LinkedOmics database. Results A total of 340 DEGs were obtained from the intersection of DEGs from the four GEO datasets， including 127 upregulated genes and 213 downregulated genes. After screening with the STRING database and Cytoscape software， the key core genes with the highest scores were secreted phosphoprotein 1 （SPP1） and transforming growth factor beta 1 （TGFB1）. The GEPIA database analysis results showed that compared with esophageal normal tissue， the expression levels of SPP1 and TGFB1 mRNA in cancer tissue were significantly increased （P<0.01）. The 1-year， 3-year， and 5-year overall survival of the EAC patients in SPP1 low expression group was higher than those in SPP1 high expression group （HR=10.1， P<0.05； HR=3.09， P<0.05； HR=2.32， P<0.05）， and the 5-year overall survival of the EAC patients in TGFB1 low expression group was higher than that in TGFB1 high expression group （HR=2.36， P<0.05）. The UALCAN database analysis results showed that compared with esophageal normal tissue， the expression levels of SPP1 and TGFB1 mRNA in cancer tissue of the EAC patients with stage Ⅱ-Ⅲ and N1-N2 lymph node metastasis were significantly increased （P<0.01）.The TIMER analysis results showed that the expression levels of SPP1 and TGFB1 mRNA in cancer tissue of the EAC patients were positively correlated with the infiltration of macrophages （r=0.353，P<0.01； r=0.187，P<0.05） and dendritic cells （r=0.236，P<0.01； r=0.221，P<0.01）. The GO and KEGG pathway enrichment analysis results showed that SPP1， TGFB1， and their top 50 positively correlated genes mainly participated in the biological processes such as cell migration， cell activity， and angiogenesis， and signaling pathways such as tumor proteoglycans， extracellular matrix （ECM）-receptor interaction， and phosphatidylinositol 3-kinase （PI3K）/protein kinase B （AKT）. Conclusion SPP1 and TGFB1 are closely associated with clinical staging， lymph node metastasis， and overall survival of the EAC patients. High expressions of SPP1 and TGFB1 may lead to the infiltration of the macrophages and dendritic cells， and change the tumor microenvironment. SPP1 and TGFB1 may become new targets for the diagnosis and treatment of EAC.

Objective To discuss the effect of the small ubiquitin-like modifier-specific protease 1 （SENP-1）/hypoxia-inducible factor 1α （HIF-1α） pathway on chronic intermittent hypoxia （CIH）-induced vascular endothelial injury in the rats， and to clarify the related mechanism. Methods The SD rats were randomly divided into control group and CIH group， and then the rats in each group were further divided into 2， 4， and 6-week subgroups， and there were 8 rats in each subgroup. The rats in CIH group were exposed to CIH in a CIH chamber to induce CIH and create the obstructive sleep apnea hypopnea syndrome （OSAHS） models， while the rats in control group were exposed to normoxic conditions.The serum and thoracic aorta tissue of the rats in various groups were collected at each time point. HE staining was used to observe the thoracic aorta vascular injury of the rats in various groups； ELISA method was used to detect the levels of nitric oxide （NO）， endothelin-1 （ET-1）， von Willebrand factor （vWF）， and thrombomodulin （TM） in serum of the rats in various groups； Western blotting method was used to detect the expression levels of SENP-1， HIF-1α， and vascular endothelial growth factor A （VEGFA） proteins in thoracic aorta tissue of the rats in various groups.In vitro， the aortic endothelial cells （rAECs） of the rats were cultured and infected with SENP-1 shRNA adenovirus （sh-SENP-1） to construct the cell line with low expression of SENP-1. The CIH was used to induce the vascular endothelial cell injury， and the cells were divided into CIH group， CIH+sh-NC group， and CIH+sh-SENP-1 group； control group was set up separately. CCK-8 method was used to detect the proliferation activities of the cells in various groups； ELISA method was used to detect the activities of lactate dehydrogenase （LDH） in the supernatant and the levels of NO， ET-1， malondialdehyde （MDA）， and activities of superoxide dismutase （SOD） in the cells in various groups； flow cytometry was used to detect the apoptotic rates of the cells in various groups； Western blotting method was used to detect the expression levels of SENP-1， HIF-1α， and VEGFA proteins in the cells in various groups. Results With the extension of CIH induction time， compared with control group， the thoracic aorta endothelium in CIH group gradually became rough and significantly thickened， the level of serum NO of the rats in CIH group was decreased （P<0.05）， and the levels of serum ET-1， vWF， and TM， and the expression levels of SENP-1， HIF-1α， and VEGFA proteins in thoracic aorta tissue were increased （P<0.05）. Compared with control group， the proliferation activity of the cells in CIH group was decreased （P<0.05）， the LDH activity in the supernatant， the levels of ET-1， MDA， and the apoptotic rate in the cells were increased （P<0.05）， while the levels of NO and activity of SOD in the cells were decreased （P<0.05）， and the expression levels of SENP-1， HIF-1α， and VEGFA proteins in the cells were increased （P<0.05）. Compared with CIH group， the proliferation activity of cells in CIH+sh-SENP-1 group was increased （P<0.05）， the activity of LDH in the supernatant， the levels of ET-1， MDA， and the apoptotic rate of the cells were decreased （P<0.05）， while the level of NO and activity of SOD in the cells were increased （P<0.05）， and the expression levels of SENP-1， HIF-1α， and VEGFA proteins were decreased （P<0.05）. Conclusion The SENP-1/HIF-1α pathway is highly activated in the thoracic aorta injury tissue of the rats induced by CIH. Silencing SENP-1 expression can reduce CIH-induced vascular endothelial cell injury， and its mechanism may be related to downregulating the activation level of SENP-1/HIF-1α pathway.

Objective To observe the effect of human mesenchymal stem cells （hMSCs） conditioned medium （CM） co-cultured with the human liposarcoma SW872 cells on the proliferation and migration of the tumor cells， and to discuss the effect of hMSCs CM on the liposarcoma cells and the possible mechanism. Methods The hMSCs were cultured in vitro and transfected with either lentiviral vector control shNS （control group） or lentiviral shRNA targeting Yes-associated protein （YAP） （shYAP-hMSCs group） by lentiviral methods. The expression levels of YAP mRNA and protein in the hMSCs in various groups were detected by real-time fluorescence quantitative PCR （RT-qPCR） and Western blotting methods. The CM was then harvested. The SW872 cells were cultured in vitro and divided into control group （normal culture）， hMSCs CM group， and shYAP-hMSCs CM group. The proliferation activities of the cells in various groups were detected by CCK-8 assay； the apoptotic rates of the cells in various groups were detected by flow cytometry； the scratch healing rates of the cells in various groups were detected by cell scratch assay； the expression levels of YAP， matrix metallopeptidase-9 （MMP-9）， and cyclin D1 proteins in the cells in various groups were detected by Western blotting method. Results Compared with control group， the expression levels of YAP mRNA and protein in the cells in shYAP-hMSCs group were decreased （P<0.01）， indicating the successful establishment of a stable transfected cell line. The CCK-8 assay results showed that compared with control group， the proliferation activity of the cells in hMSCs CM group was increased （P<0.05）， and the proliferation activity of the cells in shYAP-hMSCs CM group was decreased （P<0.01）. The flow cytometry results showed that compared with control group， there was no significant change in the apoptotic rate of the cells in hMSCs CM group （P>0.05）， while the apoptotic rate of the cells in shYAP-hMSCs CM group was increased （P<0.01）. The cell scratch assay results showed that compared with control group，the scratch healing rate of the cells in hMSCs CM group was increased （P<0.05）， and the scratch healing rate of the cells in shYAP-hMSCs CM group was decreased （P<0.01）. The Western blotting results showed that compared with control group， there were no significant differences in the expression levels of YAP， MMP-9， and cyclin D1 proteins in the cells in hMSCs CM group （P>0.05）， while the expression levels of YAP， MMP-9， and cyclin D1 proteins in the cells in shYAP-hMSCs group were decreased （P<0.05 or P<0.01）. Conclusion The hMSCs regulate the proliferation and migration of the human liposarcoma SW872 cells， and its mechanism may be related to the expression of YAP.

Objective To investigate the effect of myogenic differentiation protein 1 （Myod1） on the proliferation inhibition and apoptosis of the SH-SY5Y cells induced by oxygen-glucose deprivation （OGD）， and to elucidate its mechanism. Methods Real-time quantitative fluorescence PCR （RT-qPCR） method was used to detect the mRNA levels of Myod1 and long non-coding RNA （lncRNA） small nucleolar RNA host gene 15 （SNHG15） in peripheral blood of the subjects in normal group and the patients in ischemic cerebral infarction group as well as the normal cultured SH-SY5Y cells（control group） and the cells in OGD model （OGD group）. After transfecting SH-SY5Y cells with si-Myod1， pcDNA3.0-Myod1， si-SNHG15， pcDNA3.0-SNHG15、si-NC， Vector， miR-NC， and miR-24-3p mimics， the cells were treated with OGD， and then the SH-SY5Y cells were divided into control group， OGD group， OGD+Vector group， OGD+Myod1 group， OGD+si-NC group， OGD+si-Myod1 group， OGD+si-SNHG15 group， OGD+si-SNHG15+Vector group， OGD+si-SNHG15+Myod1 group， OGD+miR-NC group， OGD+miR-mimics group， OGD+miR-mimics+Vector group， and OGD+miR-mimics+SNHG15 group. CCK-8 method was used to detect the cell activities in various groups； 5-ethynyl-2'-deoxyuridine （EdU） staining was used to detect the rates of EDU positive cells in various groups； the rates of TdT-mediated dUTP nick end labeling （TUNEL） positive cells in various groups were detected by TUNEL staining； Western blotting method was used to detect the expression levels of cleaved caspase-3， cleaved caspase-9， B-cell lymphoma 2 （Bcl-2） and Bcl-2 associated X protein （Bax） proteins in the cells in various groups； the association between Myod1 and SNHG15 was evaluated by chromatin immunoprecipitate （CHIP）； dual luciferase reporter gene experiment was used to evaluate the targeting relationships between Myod1 and SNHG15 as well as SNHG15 and miR-24-3p. Results Compared with normal control group， the expression levels of Myod1 and SNHG15 mRNA in peripheral blood of the patients in ischemic cerebral infarction group were significantly increased （P<0.05）. Compared with control group， the expression levels of Myod1 and SNHG15 mRNA in the SH-SY5Y cells in OGD group were significantly increased （P<0.05）. Compared with OGD group， the cell activities and rates of EdU positive cells in OGD+Myod1 group at 48 and 72 h were decreased （P<0.01）， and the rates of TUNEL positive cells were increased （P<0.05）； the cell activities and rates of EdU positive cells in OGD+si-Myod1 group were increased （P<0.05）， while the rates of TUNEL positive cells were decreased （P<0.01）. Myod1 binded to the promoter sequence of SNHG15. SNHG15 could absorb miR-24-3p， and there were target relatronships between Myod1 and SNHG15 as well as SNHG15 and miR-24-3p. After SNHG15 knockdown， compared with OGD group， the cell activities and rates of EdU positive cells in OGD+si-SNHG15 group at 48 and 72 h were increased （P<0.01）， and the rates of TUNEL positive cells were decreased （P<0.01）， the expression levels of Bax， cleaved caspase-3 and cleaved caspase-9 proteins were decreased （P<0.01）， and the expression levels of Bcl-2 protein were increased （P<0.01）. Compared with OGD+si-SNHG15 group， the cell activities and rates of EdU positive cells in OGD+si-SNHG15+Myod1 group at 48 and 72 h were decreased （P<0.05）， the rates of TUNEL positive cells were （P<0.05）， the expression levels of Bax， cleaved caspase-3， and cleaved caspase-9 proteins were increased （P<0.05）， and the expression levels of Bcl-2 were decreased （P<0.05）. After over-expression of miR-24-3p and SNHG15， compared with OGD group， the cell activities and rates of EdU positive cells in OGD+miR-mimics group at 48 and 72 h were increased （P<0.01）， the rates of TUNEL positive cells were significantly decreased （P<0.01）， the protein expression levels of Bax， cleaved caspase-3 and cleaved caspase-9 were decreased （P<0.05）， and the expression levels of Bcl-2 were increased （P<0.01）. Compared with OGD+miR-mimics group， the cell activities and rates of EdU positive cells in OGD+miR-mimics+SNHG15 group at 48 and 72 h were decreased （P<0.05）， and the rates of TUNEL positive cells were increased （P<0.05）， the expression levels of Bax， cleaved caspase-3 and cleaved caspase-9 proteins were increased （P<0.05）， and the expression levels of Bcl-2 protein were decreased （P<0.05）. Conclusion Myod1 can promote the proliferation inhibition and apoptosis of OGD-induced SH-SY5Y cells by binding to the SNHG15 promoter region and then absorbing miRNA-24.

Objective To discuss the effect of exosome （Exo） microRNA-761 （miR-761） on the epithelial-mesenchymal transition （EMT） process of the osteosarcoma （OS） cells by regulating tumor-associated macrophage （TAM） polarization， and to clarify its related mechanism. Methods The miR-761 plasmid and negative control （miR-NC） plasmid were transfected into the HEK293 cells， and the non-transfected cells were regarded as control group. The transfection efficiency was detected using real-time fluorescence quantitative PCR （RT-qPCR） method.The Exo containing miR-761 was isolated， and the morphology of Exo was observed by transmission electron microscope. The concentration and size distribution of Exo samples were detected by nanoparticle analyzer， and the expression of Exo surface marker protein was detected by Western blotting method.The human monocyte leukemia THP-1 cells were stimulated with phorbol 12-myristate 13-acetate （PMA） to become the M0 macrophages， which were then treated with Exo containing miR-761 and co-cultured with the OS MG63 cells to establish the co-culture system. The experiment was divided into M0 group， TAM group， miR-761 NC group， and miR-761 Exo group. The M0 macrophages were collected from various groups， and the positive rates of M1 macrophage marker CD86 and M2 macrophage marker CD206 in various groups were detected by flow cytometry； the protein expression levels of M1 macrophage secreted factors interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α） and M2 macrophage secreted factors interleukin-10 （IL-10） and transforming growth factor-β1 （TGF-β1） in various groups were detected by Western blotting method. The M0 macrophages were treated with Exo containing miR-761 and co-cultured with MG63 cells to establish the co-culture system. The experiment was divided into control group， TAM group， miR-NC Exo+TAM group， and miR-761 Exo+TAM group. The MG63 cells in various groups were collected， and the fluorescence intensities of E-cadherin and Vimentin in the MG63 cells in various groups were observed by immunofluorescence staining； the expression levels of E-cadherin， Vimentin， and EMT regulation-related transcription factors Twist1， Snail， and Slug proteins in the cells in various groups were detected by Western blotting method；the numbers of invasion and migration cells in various groups were detected by Transwell chamber assay. Results The HEK293 cells containing miR-761 were successfully obtained by transfection experiments， and the Exo was isolated. Compared with M0 group， the positive rate of CD86 of the macrophages in TAM group was decreased （P<0.05）， while the positive rate of CD206 was increased （P<0.05）， the expression levels of IL-1β and TNF-α proteins were decreased （P<0.05）， while the expression levels of IL-10 and TGF-β1 proteins were increased （P<0.05）. Compared with TAM group， the positive rate of CD86 of the macrophages in miR-761 Exo group was increased （P<0.05）， while the positive rate of CD206 was decreased （P<0.05）， the expression levels of IL-1β and TNF-α proteins were increased （P<0.05）， while the expression levels of IL-10 and TGF-β1 proteins were decreased （P<0.05）. Compared with control group， the fluorescence intensity of E-cadherin in the MG63 cells in TAM group was decreased， while the fluorescence intensity of Vimentin was increased， the expression level of E-cadherin protein was decreased （P<0.05）， while the expression levels of Vimentin， Twist1， Snail， and Slug proteins were increased （P<0.05）， and the numbers of invasion and migration cells were increased （P<0.05）. Compared with TAM group， the fluorescence intensity of E-cadherin in the MG63 cells in miR-761 Exo+TAM group was increased， while the fluorescence intensity of Vimentin was decreased， the expression level of E-cadherin protein was increased （P<0.05）， while the expression levels of Vimentin， Twist1， Snail， and Slug proteins were decreased （P<0.05）， and the numbers of invasion and migration cells were decreased （P<0.05）. Conclusion The exo-delivered miR-761 can inhibit the EMT process of the OS cells， thereby inhibiting the cell migration and cell invasion； its mechanism may be related to regulating TAM polarization.

Objective To preliminarily predict the potential pathways and targets of Xiaoban Tongmai Formula in anti-atherosclerosis （AS） by network pharmacology analysis， and to verify its possible mechanism combined with in vitro cell experiment. Method The databases including Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）， GeneCards， Swiss Target Prediction， and Uniprot were used to collect the information on active compounds and corresponding targets of Xiaoban Tongmai Formula to construct the “compound-target-disease” network. The potential targets and pathways were predicted by protein-protein interaction （PPI） network， and the intersection targets were subjected to Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis.The human aortic vascular smooth muscle cells （HA-VSMCs） were cultured and identified in vitro， and the abnormal proliferation of HA-VSMCs were induced by oxidized low-density lipoprotein（ox-LDL） and identified； MTT method was used to detect the proliferation activities of the HA-VSMCs in various groups after treated with different concentrations of Xiaoban Tongmai Formula；the safety of Xiaoban Tongmai Fang was confirmed. The HA-VSMCs were divided into blank group， model group （the abnormal proliferation of HA-VSMCs was induced）， rosuvastatin group （treated with 4 μmol·L^-1 rosuvastatin after inducing the abnormal proliferation of HA-VSMCs）， and low， medium， and high doses of Xiaoban Tongmai Formula groups （treated with 0.025， 0.050， and 0.100 mg·L^-1 Xiaoban Tongmai Formula after inducing the abnormal proliferation of HA-VSMCs）；enzyme-linked immunosorbent assay （ELISA） was used to detect the levels of monocyte chemotactic protein-1（MCP-1）， interleukin-6（IL-6）， and interleukin-8（IL-8） in supernatant of the HA-VSMCs in various groups； real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the expression levels of nuclear factor kappa-B（NF-κB） p65 mRNA and fibroblast growth factors 2（FGF2） mRNA in the HA-VSMCs in various groups； Western blotting method was used to detect the expression levels of NF-κB p65 and FGF2 proteins in the HA-VSMCs in various groups. Results Xiaoban Tongmai Formula contained 103 active ingredients that exert anti-AS effect by acting on 189 target genes. The potential targets included IL-6， IL-8， vascular endothelial growth factor A（VEGFA）， nuclear factor kappa B1（NF-κB1）， and RELA （NF-κB p65）. The GO functional analysis and KEGG pathway enrichment analysis results showed that Xiaoban Tongmai Formula exerted anti-AS effects by regulating lipid metabolism， hypoxia-inducible factor-1（HIF-1）， epidermal growth factor（EGF）， phosphatidylinositol 3-kinase（PI3K）/protein kinase B（Akt）， and NF-κB signaling pathways.The cell morphology and immunofluorescence staining results confirmed that the cells were HA-VSMCs. The oil red O staining results showed numerous red lipid droplets， indicating successful modeling. The MTT assay results showed that Xiaoban Tongmai Formula had no significant effect on the proliferation rate of HA-VSMCs within a certain dose range， indicating good safety. The ELISA results showed that compared with model group， the levels of MCP-1 and IL-6 in supernatant of the HA-VSMCs in rosuvastatin group and different doses of Xiaoban Tongmai Formula groups were decreased （P<0.05 or P<0.01）， and the levels of IL-8 in supernatant of the HA-VSMCs in 0.050 and 0.100 mg·L^-1 Xiaoban Tongmai Formula groups were decreased （P<0.01）； compared with rosuvastatin group， the levels of MCP-1 in supernatant of the HA-VSMCs in different doses of Xiaoban Tongmai Formula groups were decreased （P<0.01）， and the levels of IL-8 in supernatant of the HA-VSMCs in 0.050 and 0.100 mg·L^-1 Xiaoban Tongmai Formula groups were decreased （P<0.01）. Compared with model group， the expression levels of NF-κB p65 mRNA in the HA-VSMCs in rosuvastatin group and different doses of Xiaoban Tongmai Formula groups were decreased （P<0.01）， and the expression levels of FGF2 mRNA in the HA-VSMCs in rosuvastatin group and 0.050 and 0.100 mg·L^-1 Xiaoban Tongmai Formula groups were decreased （P<0.01）； compared with rosuvastatin group， the expression levels of NF-κB p65 and FGF2 mRNA in the HA-VSMCs in 0.050 and 0.100 mg·L^-1 Xiaoban Tongmai Formula groups were decreased （P<0.05 or P<0.01）. Compared with model group， the expression levels of NF-κB p65 and FGF2 proteins in the HA-VSMCs in rosuvastatin group and different doses of Xiaoban Tongmai Formula groups were decreased （P<0.01）； compared with rosuvastatin group， the expression levels of NF-κB p65 protein in the HA-VSMCs in 0.050 and 0.100 mg·L^-1 Xiaoban Tongmai Formula groups were decreased （P<0.01）， and the expression level of FGF2 protein in the HA-VSMCs in 0.100 mg·L^-1 Xiaoban Tongmai Formula group was decreased （P<0.01）. Conclusion Xiaoban Tongmai Formula has anti-inflammatory effect， inhibitory effect on the proliferation of HA-VSMCs， and anti-AS effect，and its mechanism may be related to the inactivation of NF-κB/FGF2 pathway.