亚硝基化谷胱甘肽还原酶(GSNOR): 一个调控炎症反应的新分子

2014-01-03 吴凯源 张玉英 粟文婷 陈畅 生物化学与生物物理学进展

    炎症因子的表达调控是炎症反应的关键步骤,与自身免疫疾病以及癌症等密切相关.一氧化氮(nitric oxide,NO)在炎症因子表达调控中具有重要作用,但已有的研究多关注于NO合成对炎症因子的调控作用,而对NO代谢的作用知之甚少.亚硝基化谷胱甘 肽还原酶(S-nitrosoglutathione reductase,GSNOR)是体内NO信号通路代

    炎症因子的表达调控是炎症反应的关键步骤,与自身免疫疾病以及癌症等密切相关.一氧化氮(nitric oxide,NO)在炎症因子表达调控中具有重要作用,但已有的研究多关注于NO合成对炎症因子的调控作用,而对NO代谢的作用知之甚少.亚硝基化谷胱甘 肽还原酶(S-nitrosoglutathione reductase,GSNOR)是体内NO信号通路代谢调控的关键蛋白.本研究发现脂多糖(lipopolysaccharide,LPS)在 RAW264.7细胞中上调诱导型一氧化氮合酶(inducible nitric oxide synthase,iNOS)的同时下调GSNOR的转录和蛋白质表达,该下调作用依赖MEK1/2、p38和PI3K信号通路.抑制GSNOR可促进 LPS诱导的炎症因子IL-1β、IL-6和TNF-α表达,而过表达GSNOR作用相反.抗炎症药物曲古抑菌素A (trichostatin A,TSA)能够挽回LPS对GSNOR的下调作用,并且GSNOR抑制剂削弱了TSA对炎症因子IL-6和TNF-α转录的抑制效应.这些结果表 明:GSNOR

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    2014-01-18 zhaojie88
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