【摘要】 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。更多还原

【Abstract】 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,including sham group(Group S),model group(Group M),model + positive control group(Group N),and model + notoginsenoside-Rg1 25,50 and 100 mg /kg groups(Group RL,Group RM and Group RH).The Middle cerebral artery occlusion-reperfusion model was induced by clue-blocked method(blocking arterial flow for 2 hours,reperfusion for 24hours).The drugs were administered intraperitoneally twice a day.The rats in Group S and M were given with normal saline;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.更多还原