摘要
目的 探讨大鼠局灶性脑缺血再灌注损伤后血管内皮细胞凋亡及其与 Bcl- 2蛋白表达的关系。方法 采用原位末端标记法和免疫组化法分别观察脑缺血再灌注 2 h、6 h、12 h、2 4h、2 d、3d、7d、14d和 2 1d等时间点血管内皮细胞凋亡和 Bcl- 2蛋白的表达。结果 (1)脑缺血再灌注 2 h在缺血周围区即有凋亡内皮细胞出现 ,12~ 2 4h达高峰 ,之后逐渐下降 ,至 2 1d与假手术组已无显著性差异。 (2 )脑缺血再灌注后 2 h在缺血周围区内皮细胞 Bcl- 2开始表达 ,12~ 2 4h达高峰 ,之后逐渐下降 ,至 14d接近假手术组水平。(3) Bcl- 2蛋白表达时相变化与内皮细胞凋亡基本一致。结论 脑缺血再灌注损伤中凋亡是血管内皮细胞的死亡形式之一 ,Bcl- 2蛋白具有抑制缺血再灌注后血管内皮细胞凋亡的作用。
Objective To study the apoptosis and the expression of Bcl 2 protein of endothelial cells after focal cerebral ischemia/reperfusion in rats. Methods Coronal sections of brain were analyzed using an in situ terminal deoxynucleotdyl transferase mediated biotinylated deoxyuridine triphosphate nick end labeling to detect apoptotic endothelial cells. The Bcl 2 protein were detected by immunohistochemical staining methods after reperfusion (2,6,12,24hours and 2,3,7,14,21 days). Results (1)Apoptotic endothelial cells in the ischemic penumbra were observed 2h after reperfusion of MCAO,peaked at 24h,and decreased successfully to controlled level at 21d. (2)The Bcl 2 protein began to express 2h after reperfusion,peaked at 12 24h,and declined gradually to controlled level at 14d. (3)The time phase pattern of Bcl 2 is similar to that of cell apoptosis. Conclusion Apoptosis is a pattern of endothelial cell death after reperfusion of MCAO. Bcl 2 protein play an inhibit role in the process of apoptosis of endothelial cells.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2001年第3期151-154,共4页
Journal of Apoplexy and Nervous Diseases
基金
山东省自然科学基金资助项目 ( Q97C0 112 5 )