五味子乙素调控小神经胶质BV-2细胞氧化应激损伤的机制研究

    Protective Effects of Schisandrin B on Oxidative Stress in BV-2 Microglial Cells

    • 摘要: 目的 研究五味子乙素对H2O2诱导小神经胶质BV-2细胞氧化应激损伤的保护作用,并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,将细胞分为正常对照组、模型组、五味子乙素10,20,40 μmol·L-1组。CCK8试剂盒检测五味子乙素对细胞存活率的影响,相关试剂盒检测细胞匀浆中MDA、NO含量及SOD活性,免疫印迹方法检测Jak2、p-Jak2、State3、p-State3、HO-1及SOD1蛋白表达水平。结果 与模型组相比,不同剂量的五味子乙素可明显增加细胞的存活率、降低氧化应激产物MDA及NO的释放、增强SOD酶活性,差异均有统计学意义(P<0.05);免疫印迹结果显示五味子乙素可明显提高HO-1、SOD1蛋白水平,并抑制Jak2、State3的磷酸化水平,与模型组相比差异有统计学意义(P<0.05)。结论 五味子乙素可明显降低BV-2细胞的氧化应激损伤,其作用机制可能与抑制Jak2/State3信号通路的活化有关。

       

      Abstract: OBJECTIVE To observe the protective effect of schisandrin B on BV-2 microglia injury stimulated by H2O2, and investigate its possible mechanism. METHODS BV-2 cells were cultured in vitro and H2O2 was used to induce the oxidative stress model of cells. The cells were divided into 5 groups:control group, model group, schisandrin B treatment groups (10, 20, 40 μmol·L-1). CCK8 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 Jak2, p-Jak2, State3, p-State3, HO-1 and SOD1. RESULTS Compared with model group, the BV-2 cells relative survival rates and the activity of SOD after treatment with different concentrations of schisandrin B were significantly increased, while the expression levels of MDA and NO were significnatly decreased (P<0.05). The results of Western blot indicated that the expression levels of p-Jak2 and p-State3 were significantly decreased after treatment for schisandrin B, while the levels of HO-1 and SOD1 were greatly increased (all P<0.05). CONCLUSION Schisandrin B can significantly inhibit the oxidative stress injury of BV-2 cells and its underlying mechanism may involve in suppressing the activation of Jak2/State3 signaling pathway.

       

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