中文摘要：

目的：观察失荅剌知丸对大鼠脑缺血再灌注后皮质缺血周围区bcl-2和bax蛋白表达的影响。方法：78只SD雄性大鼠随机分为假手术组、模型组、金纳多组和失荅剌知丸组,后三组采用线栓法制备大脑中动脉闭塞（MCAO）模型,缺血2 h后再灌注,术后分12 h、24 h、72 h、7 d组,共13组,每组6只。采用免疫组化法和原位细胞凋亡检测脑组织Bcl-2、Bax蛋白表达及凋亡细胞数。结果：与假手术组比较,模型组及各药物组各时间点凋亡细胞数有显著增高（P〈0.01）,金纳多组各时点凋亡细胞数均明显少于模型组（P〈0.01）,失荅剌治丸组各时点凋亡细胞数均明显少于金纳多组（P〈0.01）。金纳多组各时点Bcl-2蛋白表达均明显高于模型组（P〈0.05）,失荅剌治丸组各时点Bcl-2蛋白表达均明显高于金纳多组（P〈0.05）。金纳多组各时点Bax蛋白表达均明显低于模型组（P〈0.05）,失荅剌治丸组各时点Bax蛋白表达均明显低于金纳多组（P〈0.05）。结论：失荅剌知丸可促进Bcl-2表达、抑制Bax表达,其发挥脑保护的作用机制可能与减少神经细胞凋亡有关。

英文摘要：

Objective：To study the effects of Shida Lazhi Wan on the expressions of Bcl-2 and Bax after focal cerebral ischemia and reperfusion.Methods：The model of middle cerebral artery occlusion（MCAO） and reperfusion was set up.Ischemia reperfusion after 2 h,Wistar male rats were randomly divided into normal group,model group,Ginaton group and Shida Lazhi Wan group.The rats in model group,Ginaton group and Shida Lazhi Wan group were killed 12 h,24 h,72 h and 7 d groups after cerebral ischemia and reperfusion.The brain sections were used for terminal deoxynucleotidyl transferase d UTP mickend labeling（TUNEL） staining and Bcl-2 and Bax immunohistochemical staining.Results：The apoptotic cells of model group on different time points significantly increased compared with that of normal group（P〈0.01） and the apoptotic cells of Ginaton group on different time points significantly decreased compared with that of model group（P〈0.01）.The apoptotic cells of Shida Lazhi Wan group on different time points significantly decreased compared with that of Ginaton group（P〈0.01）.The expression of Bcl-2positive cells in Ginaton group on different time points significantly increased compared with that in model group（P〈0.05）.The expression of Bcl-2 positive cells in Shida Lazhi Wan group on different time points significantly increased compared with that in Ginaton group（P〈0.05）.The expression of Bax positive cells in Ginaton group on different time points significantly decreased compared with that in model group（P〈0.05）.The expression of Bax positive cells in Shida Lazhi Wan group on different time points significantly decreased compared with that in Ginaton group（P〈0.05）.Conclusion：The neuroprotective effect of Shida Lazhi Wan on cerebral ischemia-reperfusion injury is related to inhibiting neuronal apoptosis and to up-regulate the expression of Bcl-2 with down-regulating the expression of Bax.