大鼠局灶性脑缺血后Bcl-2、Bax的表达与细胞凋亡的关系

Correlation between Expression of Bcl-2, Bax Protein and Apoptosis after Focal Cerebral Ischemia in Rats

目的探讨缺血性脑损伤中bcl－2基因家族与细胞凋亡的关系。方法用线栓法制成Wistar大鼠大脑中动脉（MCA）阻塞-再通模型，应用免疫组化方法和TUNEL法，分别对大鼠局灶性缺血脑组织Bcl－2、Bax免疫反应阳性细胞和凋亡细胞的分布进行观察。结果大鼠MCA闭塞2h再通48h后，TUNEL阳性细胞主要分布在梗死灶周围的内侧尾壳核和额顶部皮层，与Bcl－2和BaX阳性细胞数在该区域的明显增加基本一致。同时，额顶部皮层Bcl－2／Bax阳性细胞数的比例较其他脑区及对照组明显降低。结论Bcl－2和Bax在缺血后表达的比例对缺血性脑损伤中细胞生存与凋亡可能起重要的调控作用。

To study the relationship between expression of member of the bcl-2 gene family and apoptotic cell after cerebral ischemia. Methods The middle cerebral artery (MCA) in Wistar rats was occluded for 2 hours with the use of an intraluminal monofilament, and reperfusion instituted for 48 hours. Bcl-2.Bax immunoreactivity was examined by using immunohistochemical method. Apoptotic cell was detected by DNA fragmentation with the use of a terminal deoxynucleotidgltransferase mediated dUTP-biotin nick end-labeling (TUNEL) method using adjacent sections in the same rat brain. Results Immunoreactive Bcl-2 and Bax positive cells were markedly increased in the periphery of the infarction. The ratio of the number of Bcl-2 positive cells to the number of Bax positive cells declined as compared with the control group (P<0. 01). TUNEL positive cells were primarily localized to the ischemic frontoparietal cortex. Conclusions Altered ratio of expression of Bcl-2 to Bax may contribute to apoptotic cell death after cerebral ischemia.