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目的:探索柴胡疏肝散干预卒中后抑郁(PSD)模型大鼠海马神经细胞凋亡的机制及肝气郁结证与海马神经细胞凋亡的相关性。方法:健康雄性SD大鼠100只,随机分为3组:柴胡疏肝散组和PSD模型组各40只,正常对照组20只;除正常组外,其余2组先用线栓法制备局灶性脑缺血大鼠模型,手术1周后开始复合制备PSD大鼠模型,同时柴胡疏肝散组给予柴胡疏肝散7.875 g.kg-1 ig,PSD模型组给予蒸馏水ig,均21 d;免疫组化法检测大鼠海马组织Bcl-xs,Bcl-xl蛋白的表达。结果:与正常对照组比较,PSD模型组Bcl-xs蛋白表达升高,Bcl-xl蛋白表达下降(P<0.01);与PSD模型组比较,柴胡疏肝散组Bcl-xs蛋白表达下降(P<0.01),Bcl-xl蛋白表达升高(P<0.01)。结论:柴胡疏肝散对PSD模型大鼠海马Bcl-xs,Bcl-xl基因表达的调节作用可能是其干预海马神经细胞凋亡的机制之一;肝气郁结证是PSD的主要证型,且与海马神经细胞凋亡具有相关性。
Objective: To explore the mechanism of Chaihu Shugan San on apoptosis of hippocampal neurons in post-stroke depression (PSD) model rats and the correlation between qi stagnation syndrome and apoptosis of hippocampus neurons. Methods: 100 healthy male Sprague-Dawley rats were randomly divided into three groups: 40 in Chaihu Shugan Powder group and PSD model group, and 20 in normal control group. Except for normal group, the other two groups were prepared by thread-plug method The focal cerebral ischemia model was established in rats. One week after the operation, PSD rat model was prepared. At the same time, the Chaihu Shugan powder group was given 7.875 g.kg-1 ig, the model group was given distilled water ig, Each for 21 days. The expressions of Bcl-xs and Bcl-xl in hippocampus of rats were detected by immunohistochemistry. Results: Compared with normal control group, the expression of Bcl-xs protein and Bcl-xl protein in PSD model group decreased (P <0.01); Compared with PSD model group, the expression of Bcl-xs protein in Chaihu Shugan Powder group decreased P <0.01), the expression of Bcl-xl protein increased (P <0.01). CONCLUSION: Chaihu Shugan San regulates the expression of Bcl-xs and Bcl-xl genes in the hippocampus of PSD model rats, which may be one of the mechanisms of Chaihu Shugan San on the apoptosis of hippocampal neurons in PSD model. Liver-qi stagnation syndrome is the main syndrome of PSD And hippocampal neuronal apoptosis correlated.