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作 者:郭欣莹 郑彬[1] 阮祥才[1] GUO Xinying;ZHENG Bin;RUAN Xiangcai(Department of anesthesiology,Guangzhou First People′s Hospital,Guang-zhou Medical University,Guangzhou 510180,China)
机构地区:[1]广州医科大学附属市第一人民医院麻醉科,广州510180
出 处:《实用医学杂志》2018年第19期3168-3171,共4页The Journal of Practical Medicine
基 金:国家自然科学基金(编号:81271196)
摘 要:目的研究组蛋白去乙酰化酶4(HDAC4)核转位在异氟烷预处理抑制脂多糖诱导的炎症反应中的作用。方法对数生长期的THP-1细胞随机接受对照或1.5%异氟烷预处理6 h,然后行对照或不同浓度脂多糖刺激,Western blot法检测HDAC4在核蛋白和浆蛋白中的表达,ELISA法检测TNF-α的表达,MTS法检测细胞活力。结果脂多糖刺激增加TNF-α释放(P <0.05)、上调核蛋白内HDAC4表达(P <0.01)和下调胞浆蛋白的HDAC4表达(P <0.05),而异氟烷预处理能抑制脂多糖诱导的TNF-α增高(P <0.05)、抑制核蛋白内HDAC4表达(P <0.01)和上调胞浆蛋白HDAC4表达(P <0.05)。结论异氟烷预处理抑制脂多糖诱导的HDAC4核移位,从而抑制炎症因子的释放。Objective To explore the effect of nuclear translocation of HDAC4 on the inhibitory of inflam-matory cytokines by isoflurane preconditioning in human monocytes.Methods THP-1 cells in logarithmic growth phase were randomly treated with or without 1.5%isoflurane for 6 hours,then were stimulated with or without different concentrations of Lipopolysaccharide(LPS).The expression of HDAC4 in nuclear protein and cytoplasmic protein was detected by western blot.ELISA was used to detect the expression of TNF-α.MTS assay was used to detect cell viability.Results LPS showed a significant increase in the expression of TNF-αand HDAC4 in nuclear protein(P<0.05).Isoflurane preconditioning(1.5%)for 6 hours inhibited LPS-induced TNF-αrelease(P<0.05)and HDAC4 in nuclear proteins(P<0.01).However,cytoplasmic protein of HDAC4 increased after isoflu-rane preconditioning in LPS-induced inflammation(P<0.05).Conclusion Isoflurane preconditioning inhibits LPS-induced nuclear translocation of HDAC4,thereby suppresses the release of inflammatory factors.
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