线粒体在缺血预处理细胞凋亡中的作用

The Role of Mitochondria in Apoptosis Following Ischemic Preconditioning in Rats

目的 研究缺血预处理对急性心肌缺血 /再灌注细胞凋亡的影响及线粒体在其中的作用。方法 用在体心肌缺血 /再灌注模型 ,将实验动物分为对照、缺血 /再灌注、缺血预处理 3组。分别观察线粒体超微结构 ,用原位末端标记 (TUNEL)法测定凋亡心肌细胞和用免疫组化法测定Bcl 2蛋白表达。结果 与缺血 /再灌注组相比 ,缺血预处理能保护线粒体超微结构 ,减小凋亡心肌细胞百分数 (P <0 .0 1)及增加Bcl 2蛋白表达的光密度值(P <0 .0 1)。结论 缺血预处理通过保护线粒体超微结构及上调跨线粒体膜的Bcl 2蛋白表达而抑制心肌缺血

Objective To study the effect of ischemic preconditioning(IPC)on apoptosis following acute ischemia/reperfusion(I/R)and the role of mitochondria in it. Methods 24 SD rats, weighing 180～220g, were divided into 3 groups: control group, I/R group and IPC group.The mitochondrial ultramicrostructure of the above groups was observed respectively. The apoptotic myocardial cells were detected by TdT mediated dUTP biotin nick end labeling(TUNEL) and the expressions of Bcl 2 protein were measured by immunohistochemical technique. Results Compared with I/R group,IPC protected the mitochondrial ultramicrostructure, diminished the percentage of apoptotic myocardial cells(7.979 versus 27.195,n=6 in each group;P<0.01) and enhanced the OD value of Bcl 2 protein (0.136±0.018 versus 0.067±0.011;n=8 in each group;P<0.01).Conclusion IPC can inhibit the apoptosis following myocardial I/R by increasing the expressions of Bcl 2 protein which cuts through mitochondrial membrane and protecting the mitochondrial ultramicrostructure.