目的 探讨肝内糖蛋白 130（glycoprotein 130，gp130）在急性肝损伤中表达的变化及其对肝 细胞凋亡的影响及机制。方法 首先通过四氯化碳（carbon tetrachloride，CCl4）诱导小鼠急性肝损伤，检测肝内 gp130 表达、内质网应激（endoplasmic reticulum stress，ERS；以 Caspase⁃12标记）、细胞凋亡(以Cleaved caspase⁃3表达及TUNEL综合评估)的变化；其次通过4⁃苯基丁酸（4⁃phenylbutyric acid，PBA；ERS 抑制剂）干预小鼠，探讨ERS对肝内 gp130 表达的影响；最后敲减模型小鼠肝内 gp130 表达，探讨 gp130 对肝损伤、 肝细胞凋亡的影响及作用机制。结果 模型小鼠肝内 gp130 表达上调，ERS 及细胞凋亡信号显著激活 （P < 0.05）；PBA 减低肝内 gp130 表达，减轻肝细胞凋亡反应（P < 0.05）；肝内 gp130 的下调加重了 CCl4诱导 的小鼠肝损伤、ERS和肝细胞凋亡反应（P < 0.05）。结论 在急性肝损伤中ERS促进肝内gp130表达上调； gp130的上调有利于减轻肝损伤，机制可能与负性调控ERS 介导的肝细胞凋亡有关。

Objective To investigate the changes in the expression of intrahepatic glycoprotein 130 （gp130）in acute liver injury and its effect on hepatocyte apoptosis and its mechanism. Method First，carbon tetrachloride（CCl4）was used to induce acute liver injury in mice to detect changes in the expression of gp130 in the liver，endoplasmic reticulum stress（ERS；labeled with caspase⁃12），and apoptosis（with cleaved caspase⁃3 expression and TUNEL comprehensive evaluation）；Secondly，4⁃phenylbutyric acid（PBA；ERS inhibitor）was used to intervene in mice to explore the effect of ERS on the expression of gp130 in the liver；Finally，the expression of gp130 in the liver of the model mice was knocked down，and the effect and mechanism of gp130 on liver injury and hepatocyte apoptosis were explored. Result The expression of gp130 in the liver of model mice is up⁃regulated， and ERS and apoptosis signals are significantly activated（P < 0.05）；PBA reduces the expression of gp130 in the liver and reduces the apoptotic response of hepatocytes（P < 0.05）；the down⁃regulation of gp130 aggravated the CCl4⁃induced liver injury，ERS，and hepatocyte apoptosis in mice（P < 0.05）. Conclusion ERS promotes the up⁃ regulation of gp130 expression in acute liver injury；up⁃regulation of gp130 is beneficial to alleviate liver injury， and the mechanism may be related to negative regulation of ERS⁃mediated hepatocyte apoptosis.