大鼠实验性心肌缺血后Fas、bcl-2的表达与心肌细胞凋亡的关系

目的 探索心肌缺血后Fas、bcl-2的表达与心肌细胞凋亡的关系。方法 结扎大鼠左侧冠状动脉造成心肌缺血,10min—7d后取心脏标本做末端脱氧核酸转移酶介导的缺口末端标记法(TUNEL)原位细胞凋亡染色、Fas、bcl-2蛋白的免疫组织化学抗生物素蛋白-生物素复合物法(ABC法)染色。结果 在时间上,心肌细胞凋亡从缺血后3h开始,36h仍较显著,7d时TUNEL法检测不到凋亡细胞;而bcl-2、Fas分别于缺血后10min和3h开始检出,持续到缺血后7d;在组织学关系上,凋亡的心肌细胞和Fas、bcl-2阳性细胞不在心肌同一区域,凋亡的心肌细胞在心肌缺血区,Fas、bcl-2表达在无明显缺血的心肌区域。结论 Fas、bcl-2的表达可能并不直接参与缺血心肌细胞凋亡的调控。

Relationship between the expression of Fas, bcl-2 and apoptosis of cardiomyocytes in experimental myocardial ischemia in rats

Objective To explore the relationship between expression of Fas, bcl-2 and apoptosis of cardiomyocytes in myocardial ischemia in rats. Methods Myocardial ischemia was experimentally induced by ligating the left coronary artery. The rats were killed from 10 minutes to 7 days after the operation. Apoptotic myocardial cells were detected by TUNEL method. The expression of Fas and bcl-2 was studied by ABC immunohistochemistry. Results Cardiomyocytic apoptosis appeared from 3 to 36 hours after ischemia. This phenomenon however could not be detected by TUNEL method 7 days after ischemia. The expression of Fas could be detected by ABC immunohistochemistry from 3 hours to 7 days after ischemia, and the expression of bcl-2 from 10 minutes to 7 days. Cardiomyocytic apoptosis and Fas / bcl-2 expression appeared in different regions of myocardium: apoptosis in the ischemic regions, while Fas and bcl-2 expression in regions without obvious ischemia. Conclusion In rats, Fas and bcl-2 may not directly regulate apoptosis of cardiomyocytes in case of myocardial ischemia.