Abstract:

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.

Key words:

glycoprotein 130, hepatocyte apoptosis, endoplasmic reticulum stress, acute liver injury, mouse model