首页> 中文期刊>国际医药卫生导报 >石菖蒲抑制脂多糖诱导的神经胶质细胞炎性反应及其机制

石菖蒲抑制脂多糖诱导的神经胶质细胞炎性反应及其机制

摘要

Objective To evaluate the effect of serum containing Acorus tatarinowii Schott (ATS)on lipopolysaccharide(LPS)-induced neuroinflammation in glia cells and its potential mechanisms.Methods Microglial activation was induced by stimulation with LPS;and the effects of ATS on the microglial activation and production of factor-alpha (TNF-αt),interleukin-6 (IL-8),interleukin-l beta (IL-1 β),and nitric oxide(NO) were investigated.The role of inducible nitric oxide synthase(iNOS) mRNA in the antiinflammatory actions of ATS in LPS-stimulated microglia was further elucidated.Results The cell viability experiments revealed that ATS did not produce cytotoxicity in microglia.ATS significantly inhibited the LPS-induced production ofTNF-α,IL-8,IL-1β,and NO (P < 0.01).The mRNA levels ofiNOS were also attenuated by ATS (P < 0.01).Conclusion The neuroprotection of ATS might relate to the inhibition of microglial inflammation.%目的 观察石菖蒲对脂多糖(lipopolysaccharide,LPS)诱导的大鼠原代神经胶质细胞炎性反应的抑制作用并探讨其可能机制.方法 分离提取大鼠原代神经胶质细胞,用LPS刺激2h后分别加入不同浓度的石菖蒲含药血清,采用硝酸还原酶法检测石菖蒲对一氧化氮的影响,运用酶联免疫吸附法(ELISA)测定培养上清液中IL-1 β、IL-8、TNF-α水平,通过实时逆转录聚合酶链反应(RT-PCR)测定细胞中诱导型一氧化氮合酶(iNOS) mRNA表达.结果 LPS能够激活神经胶质细胞,不同浓度的石菖蒲含药大鼠血清在不影响细胞存活率的情况下,可以显著降低细胞培养上清液中NO、IL-1β、IL-8、TNF-α水平,抑制细胞内iNOS mRNA表达(P<0.05).结论 石菖蒲的神经保护机制可能与抑制胶质细胞炎症反应有关.

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