【摘要】 目的　探讨脑缺血预处理后凋亡相关基因Bcl-2、Bax在海马CA1区的表达及意义。方法　采用沙土鼠双侧颈总动脉阻断缺血再灌注损伤模型。随机分为假手术组 (SH)、预处理对照组 (IC)、预处理缺血组 (IP)及脑缺血再灌注组 (IR) ;每组据再灌注时间点不同又分 1、3、5及 7d 4个亚组 ,每组 6只动物。在预定时间点行开阔法行为学检查、TUNEL法海马CA1区凋亡细胞检测 ,免疫组织化学ABC法测定Bcl -2、Bax蛋白在海马CA1区的动态变化。结果　IP可显著减少沙土鼠探索活动及海马CA1区凋亡锥体细胞数量 (与IR组相比 ,P <0 .0 1) ,诱导Bcl-2蛋白及抑制Bax蛋白表达 (与IR组相比 ,P <0 .0 1)。结论　脑缺血预处理有确切的脑保护作用 ,调控凋亡相关基因Bcl -2、Bax蛋白的表达可能是其作用机制之一更多还原

【Abstract】 ObjectiveTo investigate t he expression of apoptosis related genes Bcl-2 and Bax after cerebral ischemic preconditioning in hippocampal CA1 area and its effects. MethodsGerbils were randomly divided into sham group (SH), ischemic-preconditi oning control group (IC), ischemic-preconditioning test group (IP) and ischemia- reperfusion (without preconditioning) group (IR). Forebrain ischemia was induced by occlusion of bilateral common carotid arteries. Observations were carried ou t in each group 1 d, 3 d, 5 d and 7 d after ischemia: open field test was used t o examine the behavioral change, the apoptosis neurons in hippocampal CA1 region was counted, the expression of Bcl-2 and Bax in hippocampal CA1 area was detect ed by SABC immunocytochemical technique. ResultsThe beha vioral mark and the number of apoptosis neurons in hippocampal CA1 region were m uch less in IP group than in IR group (P<0.01). The expression of Bcl-2 was more and the expression of Bax was less in CA1 area in IP group than in IR grou p (P<0.01). ConclusionIschemic preconditioning can significantly protect neurons against cerebral ischemia, and modulating the expr ession of apoptosis related genes Bcl-2 and Bax may be one of the protective me chanisms.更多还原