摘要
目的探究Met/HGF蛋白通路抑制细胞自噬在减轻心肌缺血再灌注损伤中的作用和机制。方法鼠离体心肌细胞分为对照组、缺血再灌注(IR)组、Met转染组、Met siRNA转染组、Met转染+肝细胞生长因子(HGF)激活剂组共5组,通过转染的方法使Met过表达或不表达,进行缺血再灌注处理后提取细胞蛋白,Western blot法检测Met、HGF,下游通路蛋白AMPK、PI3K,自噬相关蛋白LC3B、Beclin-1及凋亡蛋白Bcl-2的表达水平。结果 Western blot结果显示,与对照组相比,在Met转染组及HGF激活剂组中,过表达的Met及HGF的激活能显著增加下游信号转导通路蛋白PI3K、AMPK的表达量(P<0.05),同时自噬相关蛋白LC3B、Beclin-1的表达量均明显下降(P<0.05);而在IR组及Met siRNA转染组中则呈相反趋势(P<0.05)。结论 Met/HGF通路的激活能够抑制细胞自噬并减轻心肌细胞缺血再灌注损伤。
Objective To investigate the effect and mechanism of autophagy inhibited by Met/HGF passway in alleviating myocardial ischemia and reperfusion injury. Methods Lsolated cardiomyocytes of rats were divided into 5 groups ：control group,ischemia and reperfusion（ IR） group,Met-transfection group,Met siRNA-transfection group,Met-transfection and HGF activator group. Over or less expressions of Met were controlled by the method of transfection. Cell proteins were extracted after IR injury. The expression of cell protein such as met,HGF,AMPK,PI3 K,autophagy-related protein LC3 B,Beclin-1 and apoptosis-related protein Bcl-2 were detected by Western blot. Results Compared with control group,Western blot results showed that the expression of AMPK and PI3 K increased significantly by the method of over expression of Met and activation of HGF,the expression of autophagy-related protein LC3 B and Beclin-1 decreased significantly at the same time. However,it showed an opposite trend in IR group and Met siRNA-transfection group. Conclusion Activation of the Met/HGF signal pathway inhibits autophagy and attenuates myocardial ischemia-reperfusion injury.
出处
《安徽医科大学学报》
CAS
北大核心
2017年第12期1814-1818,共5页
Acta Universitatis Medicinalis Anhui
基金
安徽省自然科学基金(编号:1508085MH145)
