目的：探讨三七皂苷Rg1对脑缺血损伤后大鼠大脑皮质、小脑和延髓Bcl-2、Bax蛋白表达的影响。方法 SD雄性大鼠随机分为6组，即假手术组、模型组、阳性对照组、三七皂苷Rg1低（25 mg/kg）、中（50 mg/kg）和高（100 mg/kg）剂量组。除假用术组外，其余组采用线栓法复制大鼠大脑中动脉阻塞再灌注模型，每天给药2次。假手术组和模型组给予等体积的生理盐水，阳性对照组给予尼莫地平（1 mg/kg），三七皂苷Rg1各组给予相应剂量的三七皂苷Rg1，均按5 mL/kg的容量腹腔注射。给药24 h后采用神经缺失症状评分法和动物死亡率，处死动物后采用免疫组化法分别检测大鼠大脑皮质、小脑和延髓Bcl-2、Bax蛋白的表达情况。结果三七皂苷Rg1各组大鼠脑缺血损伤后的死亡率和神经缺失评分明显降低，大鼠大脑皮质、小脑和延髓Bcl-2与Bax蛋白表达的比值增加，与模型组比较差异有统计学意义（P＜0.05，P＜0.01），除大脑皮质Bcl-2与Bax蛋白的比值外，三七皂苷Rg1的中剂量与低剂量比较差异有统计学意义（ P＜0.05）。在神经缺失症状评分和动物死亡率方面，三七皂苷Rg1的中、高剂量组与阳性对照组比较差异有统计学意义（P＜0.05，P＜0.01）；在大脑皮质和延髓Bcl-2/Bax方面，三七皂苷Rg1各剂量组与阳性对照组比较均差异有统计学意义（P＜0.05，P＜0.01）；在小脑的Bcl-2/Bax方面，只有三七皂苷Rg1中剂量组与阳性对照组比较差异有统计学意义（ P＜0.05）。结论三七皂苷Rg1抗脑缺血损伤的作用机制与其增加大鼠大脑皮质、小脑和延髓的Bcl-2蛋白表达，降低大鼠大脑皮质和延髓的Bax蛋白表达及上调Bcl-2与Bax的比值有关。%Objective To investigate the effects of notoginsenoside-Rg1 on Bcl-2 and Bax protein expression in cerebral cortex , cerebellum and bulbus medullae .Methods Male SD rats were randomly divided into six groups , inclu-ding sham group (Group S), model group (Group M), model+positive control group (Group N), and model+notogin-senoside-Rg1 25, 50 and 100 mg/kg groups (Group RL, Group RM and Group RH).The Middle cerebral artery occlu-sion-reperfusion model was induced by clue -blocked method ( blocking arterial flow for 2 hours, reperfusion for 24 hours).The drugs were administered intraperitoneally twice a day .The rats in Group S and M were given with normal sa-line;the rats in Group N were given with nimodipine (1 mg/kg); while the rats in Group RL, RM and RH were given with notoginsenoside-Rg1 of 25, 50, and 100 mg/kg, respectively.The neurological deficit scores and animal mortality were evaluated 24 hours after drug administration .The immunohistochemistry were used to detect the protein expression of Bcl-2 and Bax in cerebral cortex , cerebellum and medulla oblongata .Results Rats administered with notoginsenoside-Rg1 showed a significant decrease in neurological deficit scores and animal mortality than the Group M , and increased ratio of Bcl-2 and Bax protein in cerebral cortex , cerebellum and medulla oblongata (P<0.05, P<0.01).The Group RM was remarkably different compared with Group RL except the ratio of Bcl -2/Bax protein in cerebral cortex (P<0.05), and there was dose-response relationship between them .In the neurologic deficit symptom scores and animals mortality , The Group RM and Group RL were significantly different compared with Group N (P<0.05, P<0.01).In Bcl-2/Bax of cerebral cortex and medulla oblongata , all groups of notoginsenoside -Rg1 were significant different compared with Group N (P<0.05, P<0.01).In Bcl-2/Bax of cerebellar, only Group RM was significantly different compared with Group N (P<0.05).Conclusion The mechanism of notoginsenoside-Rg1 against brain ischemia injury may be related to the up-regulation of Bcl -2 protein of erebral cortex , cerebellum and bulbus medullae , and down-regulation of Bax protein as well as raise of Bcl -2/Bax of the cerebral cortex and bulbus medullae .
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