【摘要】 [目的]研究葛根素对双氧水(H2O2)诱导小神经胶质BV-2细胞氧化应激损伤的保护作用,探讨其可能的作用机制。[方法]体外常规培养BV-2细胞,用H2O2诱导细胞氧化应激损伤模型,并同时将细胞分为正常对照组、H2O2诱导模型组、H2O2+5μmol/L葛根素组、H2O2+10μmol/L葛根素组及H2O2+20μmol/L葛根素组,CCK8试剂盒检测葛根素对细胞存活率的影响,相关试剂盒检测细胞匀浆中的氧化应激产物,免疫印迹方法检测核转录因子(Nrf2)、GCLC、NQO1及HO-1蛋白表达水平。[结果] H2O2能诱导BV-2细胞氧化应激损伤;与H2O2诱导组相比,不同剂量的葛根素可明显增加细胞的存活率、降低氧化应激产物丙二醛(MDA)及一氧化氮(NO)的释放及增强超氧化物歧化酶(SOD)酶活性,差异均有统计学意义(P<0.05);免疫印迹结果显示葛根素可明显增强Nrf2的转位,并诱导GCLC、NQO1及HO-1蛋白的表达,与H2O2诱导组相比差异有统计学意义(P<0.05)。[结论]葛根素可明显降低BV-2细胞的氧化应激损伤,其作用机制可能与活化Nrf2/ARE信号通路的有关。更多还原

【Abstract】 [Objective] To investigate the protective effects of puerarin on BV-2 microglia injury stimulated by H2 O2,and investigate its possible mechanism.[Methods] BV-2 cells were cultured in vitro and H2 O2 was used to induce the oxidative stress model of cells.The cells were divided into five groups:blank control group,H2 O2 induced model group,H2 O2 plus puerarin treatment groups(5,10,20 μg/m L).CCK-8 kit was used to measure the relative survival rate of BV-2 cells and related kits were used to analyze the levels of MDA,NO and the activity of SOD.Western Blot was used to determine the expression levels of Nrf2,GCLC,NQO1 and HO-1.[Results] H2 O2 can induce oxidative stress injury on BV-2 cells.The activity of SOD after treatment with different concentrations of puerarin were significantly increased compared to H2 O2 induced model group,while the expression levels of MDA and NO were significnatly decreased compared with model group.The results of Western Blot indicated that the Nrf2 translocation was significantly increased after treatment for puerarin,and the levels of GCLC,NQO1 and HO-1 were greatly increased(P<0.05).[Conclusion] Puerarin can significantly inhibit the oxidative stress injury of BV-2 cells and its underlying mechanism may involve in activating the activation of Nrf2/ARE signaling pathway.更多还原