| 引用本文: | 吴靖,常丽英,肖娟,续蕾.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[J].中国现代应用药学,2018,35(10):1507-1510. |
| WU Jing,CHANG Liying,XIAO Juan,XU Lei.Protective Effects of Schisandrin B on Oxidative Stress in BV-2 Microglial Cells[J].Chin J Mod Appl Pharm(中国现代应用药学),2018,35(10):1507-1510. |
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| 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。 |
| 关键词: 五味子乙素 BV-2小神经胶质细胞 氧化应激 机制 |
| DOI：10.13748/j.cnki.issn1007-7693.2018.10.016 |
| 分类号:R285.4 |
| 基金项目:湖北省高等学校优秀中青年科技创新团队计划项目（T201715） |
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| Protective Effects of Schisandrin B on Oxidative Stress in BV-2 Microglial Cells |
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wu jing and xu lei
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Xiangyang Central Hospital,Department of Neurology, Xiangyang Central Hospital
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| 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. |
| Key words: schisandrin B BV-2 microglial cells oxidative stress mechanism |
