摘要
目的研究大鼠脑缺血预处理再灌注模型Bcl-2和Bax的表达。方法采用线栓法建立大鼠脑缺血预处理再灌注模型,缺血预处理后分别再灌注6h、12h、1d、2d、3d、5d和7d,免疫组化染色观察Bcl-2和Bax蛋白表达。结果Bcl-2阳性细胞数于缺血再灌注后第1d明显增加,第3d达到高峰,并维持到第7d,均明显高于对照组(均P<0·01)。不同缺血再灌注时间Bax阳性细胞数与对照组比较差异无显著性(均P>0·05)。结论上调Bcl-2表达可能是缺血预处理产生脑保护作用的机制之一。
Objective To observe the expressions of apoptosis-related proteins Bcl-2 and Bax in cerebral ischemic preconditioning-perfusion models of rats. Methods Ischemic preconditioning was induced by 20 minutes of monolateral middle cerebral artery occlusion using an intraluminal filament method in rats. The animals were perfused 6 h, 12 h, ld, 3 d, 5 d and 7 d respectively before they were sacrificed. The expressions of Bcl-2 and Bax were analyzed by immunohistochemistry staining. Results Bcl-2 positive cells increased significantly at 1 d after perfusion, reached their peak at 3 d, and maintained high level until 7 d. They were all higher than that of control group （all P 〈 0. 01 ）. There was no difference in Bax positive cells among different group （all P 〉 0. 05 ）. Conclusion Upregulation of Bcl-2 but not Bax may play a role in ischemic preconditioning protection .
出处
《临床神经病学杂志》
CAS
北大核心
2006年第1期48-49,共2页
Journal of Clinical Neurology
