实验性急性心肌梗死中Bax和Bcl-2基因对心肌细胞凋亡的调控

目的 探讨急性心肌梗死（AMI）中Bax和Bcl-2基因对心肌细胞凋亡的调控作用。方法 新西兰兔48只，随机分为不结扎冠状动脉的正常对照组及结扎冠脉后1h，2h,3h,4h,6h,8h,12h共7组。TUNEL法检测梗死区心肌细胞凋亡，免疫组化法检测Bax和Bcl-2蛋白在心肌细胞中的表达水平。结果 急性心肌梗死心肌细胞凋亡数在冠脉结扎后1h开始增多，4h达高峰，以后逐渐下降，12h己降至正常。有Bax蛋白表达的阳性心肌细胞数与心肌细胞的凋亡数呈正相关，有Bcl-2蛋白表达的阳性心肌细胞数与心肌细胞的凋亡数呈负相关。结论 AMI免梗死区心肌细胞存在明显的凋亡现象，且受Bax蛋白上调、Bcl-2蛋白质下调，两作用相反，共同调节有着心肌细胞的凋亡。

Regulation of Bax and Bcl-2 gene on the cardiocyte apoptosis in acute myocardial infarction in rabbits

Objectives To explore the regulation of Bax and Bcl 2 gene on the cardiocyte apoptosis in acute myocardial infarction in rabbits. Methods Forty eight New Zealand rabbits were enrolled in the study.A randomized design was used to assign 42 rabbits in the 7 experimental groups (including 1 h , 2 h , 3 h , 4 h , 8 h and 12 h after coronary artery occlusion)and 6 rabbits in control group ie 0 h before coronary artery occlusion.TUNEL was applied to monitor the myocytes apoptosis.Bax and Bcl 2 protein expression were measured by immunohistochemistry. Results The permillage of apoptotic myocytes in infarct area began to increase at 1 h group and achieved the peak at 4 h and then dropped to the normal gradually.The amount of mRNA expression of Bax gene began to increase at 2 h and maintained the peak from 4 h to 10 h and then dropped to the normal gradually.The positive correlation was found between the positive myocytes of the expression of Bax protein and the amount of apoptosis and a negative correlation was found between the positive myocytes of the expression of Bcl 2 protein and the amount of apoptosis. Conclusions The marked characteristic of apoptosis in myocytes of infarct area induced by AMI was found,which were up regulated and down regulated by Bax protein and Bcl 2 protein.