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  

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

作　　者：杨磊[1] 隽兆东[1] 管英俊[2] 冷昭廷[1] 张帅[1] 孙保中[2] 盛旭东[2] 

机构地区：[1]潍坊医学院附属医院心胸外科,山东潍坊261053 [2]潍坊医学院组织学与胚胎学教研室,山东潍坊261053

出　　处：《解剖科学进展》2014年第4期341-343,共3页Progress of Anatomical Sciences

基　　金：山东省教育厅基金资助(J07YE01)

摘　　要：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。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.

关 键 词：ERK1 2 BCL-2 缺血再灌注 吡格列酮 

分 类 号：R322.11[医药卫生—人体解剖和组织胚胎学]