银丹心脑通对脑缺血再灌注大鼠海马区Bcl-2表达的影响

Effect of Yindanxinnaotong on expression of Bcl-2in hippocampus region of rats after cerebral ischemia reperfusion

目的探讨银丹心脑通对脑缺血再灌注大鼠海马CA1区神经细胞凋亡的保护作用机制。方法将40只SD雄性大鼠,随机分为假手术组、模型组、对照组、药物组,每组10只。对照组及药物组造模前分别给予尼莫地平和银丹心脑通连续灌胃7d;采用线栓改良法制备大鼠大脑中动脉闭塞模型;用免疫组织化学染色法测定各组脑组织中Bcl-2的表达。结果与假手术组比较,药物组、对照组及模型组Bcl-2阳性细胞明显升高(P<0.01);与模型组比较,药物组和对照组Bcl-2阳性细胞明显升高(P<0.01);与对照组比较,药物组Bcl-2阳性细胞明显升高(P<0.01)。结论上调Bcl-2的表达,可能是银丹心脑通减少脑缺血再灌注大鼠神经细胞凋亡的作用机制之一。

Objective To study the mechanism of Yindanxinnaotong in protecting nerve cells against apoptosis in hippocampus CA1 region of rats after cerebral ischemia reperfusion （I/R）. Methods Forty male SD rats were randomly divided into sham operation group, model group, control group and drug treatment group （10 in each group）. Rats in control group and drug treatment group were treated with nimodipin and gastric yindanxinnaotong respectively for 7 days while those in sham operation group and model group were fed with isovolumic distilled water. A middle cerebral artery occlusion model was established by modified Longa occlusion. Expression of Bcl-2 was detected with immunohistochemical staining. Results The expression level of Bcb2 was significantly higher in drug treatment group,control group and model group than in sham operation group （P〈0. 01）,and in drug treatment group and control group than in model group, whats more in drug treatment group than in control group （P〈0.01）. Conclusion The upregu- lated expression of Bcl-2 in brain tissue of rats after cerebral I/R is one of the mechanisms of Yindanxinnaotong in protecting nerve cells against apoptosis.