大鼠局灶性脑缺血再灌注脑组织神经细胞凋亡与Bcl-2、Bcl-xl蛋白检测  

Detection of neuronal cell apoptosis and expression of Bcl-2, Bcl-xl protein in focal cerebral ischemia rats

作　　者：蒋杞英[1] 王志新[1] 符风英[2] 

机构地区：[1]河南大学医学院组织学与胚胎学教研室,开封475001 [2]北京大学医学部病理生理学教研室,北京100083

出　　处：《郑州大学学报（医学版）》2004年第3期428-431,共4页Journal of Zhengzhou University(Medical Sciences)

基　　金：河南省教委自然科学基础研究项目 19993 10 0 2 1

摘　　要：目的 :探讨Bcl 2、Bcl xl与神经细胞凋亡在大鼠局灶性脑缺血再灌注损伤脑组织中的表达。方法 :栓线法阻断健康雄性大鼠大脑中动脉 (MCA)血流 2h后再灌注 ,分别于再灌注 0 .5h ,3h ,6h ,1 2h ,2 4h和 4 8h断头取脑 ,在前联合处连续切片 ,分别进行TUNEL染色及Bcl 2、Bcl xl蛋白免疫组化染色。以假手术组作对照。结果 :①脑缺血区部分神经细胞发生凋亡 ,再灌注 0 .5～ 4 8h ,凋亡细胞逐渐增多 ,凋亡指数随再灌注时间的延长而逐渐升高 ,至 4 8h时达高峰。②Bcl 2、Bcl xl蛋白在脑缺血再灌注早期开始表达 ,3～ 6h达到高峰 ,2 4h开始逐渐降低 ,至 4 8h时与对照组差异无统计学意义。③凋亡细胞 ,Bcl 2及Bcl xl蛋白均分布在脑缺血梗死灶的周边 ,梗死中心区及正常区无表达。结论 :局灶性脑缺血再灌注损伤过程中神经细胞凋亡起着重要的作用 ,而Bcl 2及Bcl xl抑制神经细胞的凋亡。Aim: To investigate the relationship between neuronal apoptosis and expression of Bcl 2 and Bcl xl in cerebral focal ischemia rats . Methods: To establish the middle cerebral artery occlusion (MCAO) model of rats. The middle cerebral artery (MCA) was occluded for 2 hours and reperfused for 0.5 h,3 h,6 h,12 h,24 h or 48 h . At each time point four slices of rat brains were taken for TUNEL staining and the expression of Bcl 2 and Bcl xl protein was detected by immunohistochemistry . Results: The number of apoptotic cells increased with the development of reperfusion within 0.5～48 h, and reached peak at 48 h.Bcl 2,Bcl xl protein was strongly expressed at the beginning of reperfusion, and reached peak in 3～6 h, and gradually reduced after 24 h. Apoptosis cell,Bcl 2 and Bcl xl protein distributed in the border of cerebral ischemia area. Conclusion: The neuronal cell apoptosis may play an important role in cerebral transient focal ischemia and reperfusion,while the Bcl 2 and Bcl xl protein may inhibit the neuronal cell apoptosis.

关 键 词：细胞凋亡 BCL-2 BCL-XL 局灶性脑缺血 再灌注 大鼠 

分 类 号：R743.3[医药卫生—神经病学与精神病学]