中文摘要：

目的探讨大鼠全脑缺血/再灌注（ischemia/reperfusion,I/R）损伤后大脑海马回中Bcl-2及Bax的表达。方法将48只SD大鼠随机分为假手术（SO）组24只;全脑缺血/再灌注（I/R）组24只,采用四血管阻塞法建立大鼠全脑I/R损伤的模型。用免疫组织化学SABC法检测大鼠海马CA1区锥体细胞中Bcl-2及Bax的表达,测量其平均灰度值,用苏木精-伊红（HE）染色检测存活锥体细胞数。结果在I/R组,可见Bcl-2平均灰度值在3小时降低;Bax在3小时平均灰度值开始降低,12小时继续降低,24小时降低达到高峰,到48小时开始回升;存活神经元数目随再灌注时间的延长而减少（P均〈0.01）。结论大鼠全脑缺血/再灌注后,Bcl-2和Bax参与了脑神经元凋亡的调控。

英文摘要：

Objective To investigate the expression of Bcl-2/Bax in hippocampus after cerebral ischemia-reperfusion. Methods 48 healthy SD rats were randomly divided into 2 groups,including sham operation（SO） group（n=24） and I/R group（n= 24）. The model of global cerebral ischemia/reperfusion injury was produced by simple Pulsinelli- Brierley＇s four arteries occlusion method. Bcl-2 and Bax expression in rat hippoeampal CA1 pyramidal cells were detected with imunolistochemestry SABC assay. HE staining was performed to detect the number of surviving neurons. Results In I/R group, the average gray value of Bcl-2 began to decrease at 3h after reperfusion. The average gray value of Bax began to decrease at 3h after reperfusion, The peak was at 24h, and then gradually increased at 48h. The number of surviving neurons reduced with the extension of reperfusion （P〈0.01）. Conclusions After global cerebral ischemia/reperfusion, neurons apoptosis is regulated by Bcl-2 and Bax.