中文摘要：

目的：本研究通过建立氯化锂一匹罗卡品诱导大鼠癫痫模型，用人参皂苷Rgl（Rgl）进行干预，检测癫痫大鼠海马中的Bax、Bcl-2的表达及Rgl对其的调控作用，初步探讨Rgl对癫痫可能的神经保护机制。方法：健康成年雄性SD大鼠随机分为5组，即空白对照组，模型组，低、中、高剂量Rgl治疗组，每组20只，观察行为学变化，并于点燃后72h取脑，分别通过免疫荧光显色、免疫印迹和RT-PCR检测Bax和Bcl-2的蛋白和RNA表达情况。结果：空白组未出现癫痫发作及死亡，不同剂量的Rgl预处理组与模型组相比，大发作潜伏期时间延长。匹罗卡品诱导大鼠癫痫发作后，海马神经元的胞质内凋亡因子Bax免疫阳性反应增强，蛋白产物表达增多，抗凋亡因子Bcl-2表达减少。Rgl预处理组促凋亡因子Bax及其mRNA表达减少，抗凋亡因子Bcl-2及其mRNA表达增加。结论：癫痫发作后可引起凋亡因子的表达变化，而人参皂苷Rgl可以通过下调促凋亡因子Bax的表达，上调抗凋亡因子Bcl-2的表达，从而发挥抗癫痫的神经保护作用。

英文摘要：

Objective： To explore the protective mechanism of ginsenoside Rgl on epilepsy and detect the Bax and Bcl-2 expression in rats induced by intraperitoneal injection of pilocarpine combined with lithium chloride and treated with Rgl. Methods.. Adult male SD rats were randomly divided into five groups., control group, model group and different doses of ginsenoside Rgl （Rgl） pretreatment group. The status of seizure after intraperitoneal injection with pilocarpine was observed, and then the heads of the rats were cut to take their brains 72 hours after seizure. Expression of Bcl-2 and Bax protein was detected with Western blotting and immunofluorescence method. The mRNA levels of Bax and Bcl-2 were detected by RT- PCR. Results： Seizure and death didn＇t appear in the control group. Compared with the model group, latent period of seizure increased obviously after treatment with different doses of Rgl. Western blotting showed that the expression of Bcl-2 protein and the Bcl-2 mRNA levels in Rgl group were higher than that in the model group, and the expression of Bax protein and the Bax mRNA levels in Rgl group were lower than that in the model group. Bcl-2 positive cells in the hippocampus in the model group increased than that in Rgl group, while Bax positive cells of in Rgl group decreased. Conclusion ： Seizure can cause the activation of apoptosis factors. Rgl may play a protective role on nervous system through down-regulating the expression of Bax and up-regulating the expression of Bcl-2.