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目的探讨帕金森相关蛋白Parkin基因在肝脏缺血再灌注损伤中对细胞自噬的作用。方法采用肝门阻断法建立大鼠肝脏缺血再灌注模型,实时荧光定量聚合酶链式反应(quantitative real-time polymerase chain reaction,qRT-PCR)和Western blot法分别检测Parkin基因及蛋白表达水平在缺血再灌注前后的变化,同时检测缺血再灌注前后细胞自噬关键蛋白LC3的表达变化;构建靶向Parkin基因的RNA干扰质粒,检测下调Parkin基因表达后对缺血再灌注损伤细胞自噬的影响。结果肝脏缺血再灌注损伤后,Parkin蛋白的表达水平显著增加,同时肝细胞自噬发生显著增加。下调Parkin基因表达后,肝细胞自噬显著降低(t=11.94,P=0.003)。结论 Parkin基因能够有效诱导肝脏缺血再灌注损伤中的细胞自噬的发生,是肝脏缺血再灌注损伤的保护性基因。
Objective To investigate the role of Parkin gene in Parkinson’s disease on autophagy in liver ischemia-reperfusion injury. Methods Hepatic ischemia-reperfusion model was established by hepatic portal blockade. The expression of Parkin gene and protein were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot respectively The changes of LC3 protein before and after ischemia-reperfusion and the expression of LC3 protein of Parkinson’s disease were detected by RT-PCR. The expression of Parkin gene was detected by RNA interference and the expression of Parkin gene was detected. The impact of bite Results After hepatic ischemia-reperfusion injury, the expression of Parkin protein increased significantly, meanwhile the autophagy in hepatocytes increased significantly. After down-regulating Parkin gene expression, autophagy in hepatocytes decreased significantly (t = 11.94, P = 0.003). Conclusions Parkin gene can effectively induce autophagy in hepatic ischemia-reperfusion injury and is a protective gene for hepatic ischemia-reperfusion injury.