目的 构建环状RNA（circRNA）-微小RNA（miRNA）-信使RNA（mRNA）竞争性内源RNA（ceRNA）网络，探讨其在刀豆蛋白A诱导的自身免疫性肝炎（AIH）小鼠模型中的潜在调控机制，并验证关键基因的表达与肝损伤的关系。 方法 使用高通量数据筛选差异表达的circRNA、miRNA和mRNA，基于Pearson相关分析和Miranda程序预测miRNA与mRNA及circRNA的配对关系，构建ceRNA网络。对网络中的差异表达基因进行GO和KEGG富集分析。选取SPF级雄性C57BL/6小鼠12只，采用随机数字表法分为对照组和模型组，每组6只，模型组通过尾静脉注射刀豆蛋白A构建AIH小鼠模型，对照组注射生理盐水。通过qRT-PCR和Western Blot方法验证circ_0001577、miR-7055-3p和Akt3的表达。测定血清转氨酶（ALT、AST）和肝组织中丙二醛（MDA）及一氧化氮（NO）含量，并分析其与基因表达的相关性。计量资料两组间比较采用成组t检验。使用Spearman相关分析法分析基因表达与肝损伤指标之间的相关性。 结果 构建了包含5 795个circRNA-miRNA-mRNA配对的ceRNA网络，发现circ_0001577为中心基因。与对照组小鼠比较，模型组中的circ_0001577和Akt3表达上调，miR-7055-3p下调，差异均有统计学意义（P值均<0.05），且circ_0001577与Akt3呈正相关（r=0.861，P<0.001），miR-7055-3p与两者呈负相关（r值分别为-0.644、-0.855，P值均<0.05）。模型组小鼠肝脏Akt3蛋白表达显著高于对照组（1.04±0.10 vs 0.72±0.06，t=-6.49，P=0.001），并与circ_0001577呈正相关（r=0.579，P=0.048），与miR-7055-3p呈负相关（r=-0.891，P<0.001）。模型组小鼠血清ALT、AST和肝组织MDA、NO含量较对照组均显著增加（P值均<0.05），上述肝损伤指标与circ_0001577、Akt3呈正相关（r值分别为0.849、0.865、0.811、0.801；0.889、0.954、0.938、0.961，P值均<0.05），与miR-7055-3p呈负相关（r值分别为-0.687、-0.818、-0.833、-0.870，P值均<0.05），且与Akt蛋白表达呈正相关（r值分别为0.648、0.796、0.848、0.860，P值均<0.05）。 结论 circ_0001577通过竞争性吸附miR-7055-3p，导致Akt3抑制被解除，进而促进Akt3的表达，参与AIH的发生发展。circ_0001577及其相关通路可能成为AIH的潜在治疗靶点。

Objective To construct a circRNA-miRNA-mRNA competitive endogenous RNA （ceRNA） network，to investigate its potential regulatory mechanism in a mouse model of autoimmune hepatitis （AIH） induced by concanavalin A （ConA），and to verify the association between the expression of key genes and liver injury. Methods High-throughput data were used to identify differentially expressed circRNAs，miRNAs，and mRNAs，and the Pearson correlation analysis and the Miranda program were used to predict the pairing relationships between miRNAs and mRNAs/circRNAs and construct a ceRNA network. The gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed for the differentially expressed genes in the network. A total of 12 specific pathogen-free male C57BL/6 mice were divided into control group and model group using a random number table，with 6 mice in each group. The mice in the model group were given injection of ConA via the caudal vein to establish a mouse model of AIH，and those in the control group were given injection of normal saline. The methods of qRT-PCR and Western blot were used to validate the expression levels of circ_0001577，miR-7055-3p，and Akt3. The serum levels of alanine aminotransferase （ALT） and aspartate aminotransferase （AST） were measured，as well as the content of malondialdehyde （MDA） and nitric oxide （NO） in liver tissue，and their correlation with gene expression was analyzed. The independent-samples t test was used for comparison of continuous data between two groups，and the Spearman correlation analysis was used to investigate the correlation between gene expression levels and liver injury indicators. Results A ceRNA network containing 5 795 circRNA-miRNA-mRNA pairings was constructed，and circ_0001577 was identified as the central gene. Compared with the control group，the model group had significant increases in the expression levels of circ_0001577 and Akt3 and a significant reduction in the expression of miR-7055-3p （all P<0.05），and circ_0001577 was positively correlated with Akt3 （r=0.861，P<0.001），while miR-7055-3p was negatively correlated with circ_0001577 and Akt3 （r=-0.644 and -0.855，both P<0.05）. Compared with the control group，the model group had a significantly higher protein expression level of Akt3 in the liver （1.04±0.10 vs 0.72±0.06，t=-6.49，P=0.001），which was positively correlated with circ_0001577 （r=0.579，P=0.048） and was negatively correlated with miR-7055-3p （r=-0.891，P<0.001）. Compared with the control group，the model group had significant increases in the serum levels of ALT and AST and the content of MDA and NO in liver tissue （all P<0.05），and these liver injury indicators were positively correlated with circ_0001577 and Akt3 （r=0.849，0.865，0.811，0.801； 0.889，0.954，0.938，and 0.961，all P<0.05） and were negatively correlated with miR-7055-3p （r=-0.687，-0.818，-0.833，and -0.870，all P<0.05）； in addition，they were positively correlated with the protein expression level of Akt3 （r=0.648，0.796，0.848，and 0.860，all P<0.05）. Conclusion This study shows that circ_0001577 promotes the expression of Akt3 by competitively adsorbing miR-7055-3p and relieving the inhibition of Akt3，thereby participating in the development and progression of AIH.