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目的:探讨脑缺血再灌注(CIR)大鼠脑皮质Bax,Bcl-2和GFAP表达及川芎嗪的干预作用。方法:72只Wister大鼠随机分成假手术组,模型组,小剂量治疗组和大剂量治疗组。其中54只大鼠利用Bannister’s颈动脉血引流法复制CIR动物模型。治疗组分别向腹腔注射川芎嗪50mg/kg或100mg/kg。术后12,24,72h取脑组织,用免疫组织化学方法检测Bax,Bcl-2和GFAP(胶质纤维酸性蛋白)阳性细胞。结果:模型组Bax,Bcl-2和GFAP阳性细胞值明显高于假手术组和治疗组,Bax/Bcl-2大于1;治疗组Bax,GFAP阳性细胞数减少,Bcl-2增多,治疗大剂量组Bax/Bcl-2比值明显下降小于1。结论:川芎嗪能够下调CIR脑皮质Bax和GFAP表达和上调Bcl-2表达,说明川芎嗪通过干预基因表达发挥脑保护作用。
Objective: To investigate the expression of Bax, Bcl-2 and GFAP in cerebral cortex of cerebral ischemia-reperfusion (CIR) rats and the intervention of tetramethylpyrazine. Methods: Seventy-two Wister rats were randomly divided into sham operation group, model group, low-dose treatment group and large-dose treatment group. Fifty-four rats replicated the CIR animal model using Bannister’s carotid blood drainage. The treatment group was injected intraperitoneally with Ligustrazine 50 mg/kg or 100 mg/kg. Brain tissues were taken at 12, 24, and 72 hours after operation. Bax, Bcl-2, and GFAP (glial fibrillary acidic protein) positive cells were detected by immunohistochemistry. Results: The values of Bax, Bcl-2 and GFAP positive cells in the model group were significantly higher than those in the sham group and the treatment group, Bax/Bcl-2 was greater than 1; the number of Bax and GFAP positive cells in the treatment group was decreased, Bcl-2 was increased, and large doses were treated. The group Bax/Bcl-2 ratio significantly decreased by less than one. Conclusion: Tetramethylpyrazine can down-regulate the expression of Bax and GFAP and up-regulate the expression of Bcl-2 in cerebral cortex of CIR, indicating that tetramethylpyrazine exerts brain protection by intervening gene expression.