下调基因Trib3表达对H_2O_2诱导肝细胞凋亡的影响

Effect of Trib3 Downregulation on Hydrogen Peroxide-Induced Hepatocyte Apoptosis

目的观察Trib3基因在肝细胞氧化应激诱导凋亡中的作用及可能机制。方法建立H_2O_2诱导的肝细胞凋亡模型,瞬时转染siTrib3至人正常肝细胞系,RT-PCR及Western blot验证Trib3的表达。流式检测转染siTrib3后对H_2O_2诱导的肝细胞凋亡的影响,Western blot检测凋亡蛋白及Stat3信号通路的表达。结果在H_2O_2诱导的肝细胞氧化应激诱导凋亡模型下,Trib3的表达增加(P<0.01),下调Trib3蛋白增加H_2O_2诱导的肝细胞凋亡(P<0.01),并可激活Stat3信号通路。结论 Trib3蛋白参与了H_2O_2诱导的肝细胞凋亡,且保护H_2O_2诱导的肝细胞凋亡,其机制可能与Stat3信号通路的激活有关。

Objective To investigate the effect of Trib3 on hepatocyte apoptosis induced by oxidative stress and its underlying mechanism.Methods The model of hydrogen peroxide（H2O2）-induced hepatocyte apoptosis was established in this study.The normal human liver cells were transiently transfected with siTrib3.The expression of Trib3 was detected by RT-PCR and Western blot.The apoptosis of hepatocytes was determined by flow cytometry.The expression of apoptosis proteins and STAT3 signal pathway was measured by Western blot.Results The expression of Trib3 increased in the model of H2O2-induced hepatocyte apoptosis（P〈0.01）.Furthermore,the downregulation of Trib3 increased H2O2-induced apoptosis and activated STAT3 signal pathway in hepatocytes（P〈0.01）.Conclusion Trib3 protein protects hepatocytes from apoptosis induced by H2O2 through activating STAT3 signal pathway.