目的 研究利拉鲁肽对脂多糖（lipopolysaccharide， LPS）诱导的脓毒症小鼠脑损伤的保护作用及机制。 方法 90只C57BL/6小鼠，随机分为3组（n = 30）：对照组（Control），脓毒症组（LPS），LPS + 利拉鲁肽组（LPS + Lira）。LPS 组和LPS + Lira 组腹腔注射LPS（15 mg/kg），Control组注射等量生理盐水。LPS + Lira组小鼠在LPS注射前2天皮下注射利拉鲁肽（200 µg/kg），每天2次，连续3 d。 结果 3组小鼠的生存率、脑含水量、海马CA1区正常锥体细胞数、细胞凋亡率、氧化应激指标、炎症因子水平及相关蛋白表达水平进行比较，差异均具有统计学意义（P < 0.05）。进一步两两比较显示，LPS组比Control组的生存率降低（P < 0.05），脑含水量增加（P < 0.05），海马CA1区正常锥体细胞数减少（P < 0.05），细胞凋亡率增加（P < 0.05），氧化应激和炎症因子水平升高（P < 0.05），NLRP3、Casp1 p10、Caspase-3和Bax蛋白表达水平均增加（P < 0.05），Bcl-2表达减少（P < 0.05）。LPS + Lira组小鼠的各项指标较LPS组均明显改善（P < 0.05）。 结论 利拉鲁肽通过抑制NLRP3/Caspase-1信号通路的激活，可减轻炎症反应、氧化应激及细胞凋亡，对LPS诱导的脓毒症脑损伤具有明显保护作用。

Objective To investigate the protective effect and underlying mechanism of liraglutide on brain injury in lipopolysaccharide （LPS）-induced septic mice. Methods Ninety C57BL/6 mice were randomly divided into three groups （n = 30）： the Control group， the Sepsis group （LPS）， and the LPS + Liraglutide group （LPS + Lira）. The LPS and LPS + Lira groups received intraperitoneal injections of LPS （15 mg/kg）， while the Control group received an equal volume of normal saline. The LPS + Lira group was subcutaneously injected with liraglutide （200 µg/kg） twice daily for 3 consecutive days， starting 2 days before the LPS injection. Results Significant differences were observed among the three groups in terms of survival rate， brain water content， the number of normal pyramidal cells in the hippocampal CA1 region， apoptosis rate， oxidative stress markers， inflammatory cytokine levels， and related protein expression （P < 0.05）. Further pairwise comparisons showed that， compared to the Control group， the LPS group had a significantly reduced survival rate （P < 0.05）， increased brain water content （P < 0.05）， decreased number of normal pyramidal cells in the hippocampal CA1 region （P < 0.05）， and an elevated apoptosis rate （P < 0.05）. Additionally， oxidative stress and inflammatory cytokine levels were significantly higher （P < 0.05）， with increased expression of NLRP3， Casp1 p10， Caspase-3， and Bax proteins （P < 0.05）， and decreased expression of Bcl-2 （P < 0.05）. The LPS + Lira group showed significant improvement in all these indicators compared to the LPS group （P < 0.05）. Conclusion Liraglutide exerts a protective effect against LPS-induced septic brain injury by inhibiting the activation of the NLRP3/Caspase-1 signaling pathway， thereby reducing inflammation， oxidative stress， and apoptosis.