PI3K/AKT/Bcl-2通路在吡格列酮保护缺血再灌注损伤心肌细胞中作用的研究

目的 研究吡格列酮对缺血再灌注损伤心肌细胞的保护作用机制中PI3K/AKT/Bcl-2信号通路的作用.方法 取Wistar大鼠乳鼠心室肌细胞进行体外培养,缺氧、复氧各3 h后建立缺血再灌注损伤细胞模型.采用免疫细胞化学染色法检测细胞内Bcl-2蛋白含量,采用Western-bloting检测细胞内Bcl-2蛋白表达水平.结果 免疫细胞化学染色法及Western-bloting结果均显示：与Ⅰ组比较,P组Bcl-2表达明显增加（P〈0.05）;与P组比较,P＋Ly组Bcl-2表达明显减少（P〈0.05）.结论 吡格列酮减轻心肌缺血再灌注损伤保护机制与其激活PI3K/AKT/ Bcl-2信号通路有关.

The study on the effects of PI3K/AKT/Bcl-2 Signaling Pathway In Pioglitazone protecting Myocardial ischemia-reperfusion

Objective To study the protective mechanism of Pioglitazone on myocardial cell of ischemia - reperfusion injury. Methods New born Wistar rats hearts were isolated and cardiomyocytes were separated by trypsin digestion. The primary cardiomyocytcs were collected and incubatedin vitro. Schemia - reperfusion injury was established by 3 hours of hyopxia and 3 hours of reoxygenation subsquently. Bcl - 2 protein of intracellular content were detected by Immunocytochemical and Western - bloting. Results Immunocytochemical and Western - blotting results showed that ： compared with the I groups , the P group＇s Bcl -2 were significantly increased （P 〈 0.05 ） ; compared with the P groups , the P ＋ Ly group＇s Bcl -2 were sig- nificantly reduced （ P 〈 0.05 ）. Conclusion The Pioglitazone Reduced myocardial ischemia - reperfusion injury with the acti- vation of protective mechanisms of the PI3K/AKT/Bcl -2 signaling pathway.