【摘要】 [目的]探讨人参皂甙Rb1(GRb1)对香烟烟雾诱导大鼠神经细胞损伤的保护作用和机制。[方法]制备烟灌注大鼠模型,吸烟量分别为8、20、40支/d,12周后腹腔注射不同剂量的GRb1(10、20、40 mg/kg)。各组大鼠同时制备皮层神经细胞培养液,24 h后应用Annexin V联合流式细胞仪检测细胞凋亡率和坏死率,Western-Blot检测存活素(Survivin)的表达水平,Fura-2/AM负载及荧光标记检测神经细胞内游离Ca2+浓度。[结果]香烟烟雾刺激诱导神经细胞发生凋亡和坏死,与对照组相比凋亡率和坏死率显著增高。与对照组相比,8支/d香烟烟雾刺激使Survivin表达增强34%,20、40支/d香烟烟雾刺激使Survivin表达分别下降48%和67%;20、40 mg/kg的GRb1使细胞凋亡率分别下降30.6%和40.3%,细胞坏死率分别下降32.5%和39.4%,Survivin表达水平上调45.1%和54.8%。香烟烟雾可使神经细胞内游离Ca2+浓度显著升高,GRb1使神经细胞内Ca2+浓度显著下降(P﹤0.01)。[结论]GRb1通过抑制细胞内Ca2+超载,调节Survivin表达,减轻香烟烟雾对神经细胞的损伤。更多还原

【Abstract】 [Objective]To investigate the effects of Ginsenoside Rb1(GRb1)on rat neurotoxicity induced by cigarette smoke.[Methods]Male Wister rats were prepared under cigarette smoking for 12 weeks.The amount of cigarettes was 8,20 and 40 per day,respectively.GRb1(10,20 and 40mg/kg)was administered intra-peritoneal to rats after rat smoking for 12 weeks.Cerebral cortex neuronal cells were prepared from these rats in vitro.After 24h of GRb1 treatment,flow cytometric analysis of Annexin V(marks apoptosis)and PI(propidium iodide,marks necrosis)labeling cells.Western-Blot experiment was used to detect the expression of Survivin.The contents of free Ca2+ were determined in each group.[Results]Cigarette smoke induced cerebral cortex neuronal apoptosis and necrosis,apoptosis and necrosis rates were significantly increased compared with control group.Compared with control group,8 rami/d cigarettes increased 34% in the level of Survivin,20 or 40rami/d cigarettes decreased 48% and 67% in the level of Survivin.However,GRb1 markedly reduced apoptosis and necrosis due to toxicity of 20rami/d cigarettes compared with the vehicle-treated cigarette smoke group,the apoptosis was reduced by 30.6% and 40.3%,and necrosis was reduced by 32.5% and 39.4%,after treatment by GRb1 of 20 and 40mg/kg.Meanwhile,GRb1 obviously reversed the down-regulation of Survivin expression induced by cigarette smoking(up-regulation by 45.1% and 54.8% when compared with that of the vehicle-treated cigarette smoking group).A Ca2+ probe showed an obvious increase in the intracellular Ca2+ during cigarette smoking treatment,and GRb1 of 20 or 40mg/kg significantly showed down cigarette-induced Ca2+ influx(P﹤0.01).[Conclusion]The neuroprotective effect of GRb1 against cigarette smoke toxicity was associated with inhibition of the accumulation of intracellular Ca2+ and up-regulation of Survivin expression in cerebral cortex neurons.更多还原