缺血预处理对体外循环后心肌细胞凋亡及PI3K／Akt通路的影响

Effects of Ischemia Preconditioning on Myocardium Apoptosis and PI3K/Akt Pathway

目的:观察缺血预处理对犬体外循环术后心肌细胞凋亡以及PI3K/Akt通路的影响。方法:10只雄性健康家犬随机分为对照组和缺血预处理组。常规建立体外循环,对照组阻断主动脉60min后开放;预处理组于阻断主动脉前,夹闭主动脉2min后开放3min,反复2次。于主动脉开放90min后取心肌标本。使用TUNEL法检测心肌细胞凋亡指数,免疫组化法检测磷酸化蛋白激酶B(P-Akt)、凋亡相关蛋白BAX及Bcl-2表达情况。结果:缺血预处理可以明显减少体外循环后心肌细胞凋亡指数,降低再灌注90min后凋亡蛋白BAX/Bcl-2比值,上调磷酸化Akt表达。结论:缺血预处理抑制犬体外循环后心肌细胞凋亡,并激活再灌注后PI3K/Akt通路。

Objective： To study the effects of ischemia preconditioning on myocardial apoptosis after cardiopulmonary bypass, and to explore its effects on PI3K/Akt pathway. Methods： Ten healthy male canines undergoing CPB （cardiopulmonary bypass） were divided into two groups. In control group, CPB was founded, and aortic cross clamping （ACC） was performed for 60 minutes and then unclamped, which was conducted without any treatment. In ischemic preconditioning （IPC） group, IPC was conducted three circles with two minutes ischemia and three minutes reperfusion, unclamped for 90 minutes, then the cardiac muscle was obtained. The apoptotic index of cardiomyocyte was detected by TUNEL. Levels of phosphorated Akt （P-Akt）, BAX and Bcl-2 were detected by immunohistochemistry. Results： IPC significantly decreased myocardium apoptotic index and BAX/Bcl-2 ratio 90 minutes after reperfusion. IPC significantly increased P-Akt level at 90 minutes after reperfusion. Conclusion： IPC can limit myocardial apoptosis after the CPB. IPC can activate the PI3K/Akt pathway after reperfusion.