吡格列酮上调ERK1/2与Bcl-2在心肌细胞缺血再灌注损伤大鼠心肌细胞的表达

目的研究吡格列酮对ERK1/2与Bcl-2信号转导通路在大鼠心肌缺血再灌注损伤中的作用。方法取半日龄到一日龄Wistar大鼠幼鼠心室肌细胞进行体外培养,并建立缺血再灌注模型。体外培养的细胞分为正常对照组(C组)、缺血再灌注组(I组)、缺血再灌注组+吡格列酮处理组(P组)和P组+ERK1/2抑制剂PD98059处理组(P+Pd组)。采用Western-bloting和免疫细胞化学染色法检测细胞内Bcl-2蛋白的含量。结果 Western-bloting与免疫细胞化学法显示,I组Bcl-2蛋白表达水平高于C组(0.05),P组的Bcl-2蛋白表达高于I组,P+Pd组Bcl-2蛋白表达水平低于P组(0.05)。结论吡格列酮对心肌细胞缺血再灌注损伤的保护可能与下调ERK1/2和Bcl-2转导通路有关。

Pioglitazone upregulates the expression of ERK1/2 and Bcl-2 signal molecule in myocardial ischemia-reperfusion injury rat

Objective To study the effect of pioglitazone on the expression of ERK1/2 and Bcl-2 signal molecule to explore the protective mechanism of pioglitazone on myocardial ischemia-reperfusion injury in rats. Methods The ventricular myocytes from half-day to one-day-old Wistar rats were cultured in vitro and ischemia-reperfusion injury model was established. The ventricular myocytes were divided into normal control（C）, ischemia-reperfusion（I）,I＋pioglitazone（P） and P＋PD98059（P＋Pd） groups. The levels of Bcl-2 protein expression were detected by Western-bloting and immunocytochemistry. Results Western-bloting and immunocytochemistry showed that the expression levels of Bcl-2were increased in I group than in C group, higher in P group than in I group, but lower in P＋Pd group than in P group.Conclusion The protection effect of Pioglitazone on myocardial ischemic reperfusion injury may be related to the upregulation of ERK1/2 and Bcl-2 signal molecule.