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首页> 外文期刊>Journal of Cellular Physiology >Suppression of inducible nitric oxide generation by agmatine aldehyde: beneficial effects in sepsis.
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Suppression of inducible nitric oxide generation by agmatine aldehyde: beneficial effects in sepsis.

机译：抑制诱导一氧化氮的生成胍基丁胺醛:有利影响脓毒症。

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The induction of inducible nitric oxide synthase (iNOS) serves an important immuno-protective function in inflammatory states, but ungoverned nitric oxide (NO) generation can contribute to a number of pathologic consequences. Delineation of the mechanisms that can downregulate iNOS-generated NO in inflammation could have therapeutic relevance. Here we show that agmatine, a metabolite of arginine, inhibits iNOS mediated nitric oxide generation in cytokine stimulated cell culture preparations. This effect was not cell type specific. Increased diamine oxidase (DAO) and decreased aldehyde dehydrogenase (AldDH) activities are also representative of inflammatory settings. Increasing the conversion of agmatine to an aldehyde form by addition of purified DAO or suppression of aldehyde breakdown by inhibition of AldDH activity increases the inhibitory effects of agmatine in an additive fashion. Inhibitors of DAO, but not monoamine oxidase (MAO), decreased the inhibitory effects of agmatine, as did the addition of AldDH or reacting aldehydes with phenylhydrazine. We examined rats given lipopolysaccharide (LPS) to evaluate the potential effects of agmatine in vivo. Endotoxic rats administered agmatine prevented the decreases in blood pressure and renal function normally associated with sepsis. Agmatine treatment also increased the survival of LPS treated mice. Our data demonstrate the capacity of agmatine aldehyde to suppress iNOS mediated NO generation, and indicate a protective function of agmatine in a model of endotoxic shock. How agmatine may aid in coordinating the early NO phase and the later repair phase responses in models of inflammation is discussed. Copyright 2001 Wiley-Liss, Inc.
机译：诱导一氧化氮合酶的诱导(间接宾语)是一个重要的immuno-protective在炎症状态函数,但处于失控状态一氧化氮(NO)代可以贡献数字病理的后果。机制,可以表达下调iNOS-generated没有炎症的可能治疗的相关性。胍基丁胺,精氨酸的代谢产物抑制伊诺在细胞因子介导的一氧化氮生成刺激细胞培养的准备。没有特定的细胞类型。氧化酶(DAO)和降低醛脱氢酶(AldDH)活动也代表炎症设置。增加了转换的胍基丁胺通过添加净化刀或醛形式通过抑制抑制醛崩溃AldDH活动增加了抑制胍基丁胺的添加剂时尚的影响。抑制剂的刀,但不是单胺氧化酶(毛),减少的抑制性影响胍基丁胺,添加AldDH或醛与苯肼反应。研究大鼠给予脂多糖(LPS)胍基丁胺的潜在影响进行评估vivo防止血压和降低肾功能正常与脓毒症有关。胍基丁胺治疗也增加了的生存有限合伙人治疗老鼠。胍基丁胺醛压制伊诺的能力调解没有生成,表明保护函数的胍基丁胺的内毒素的模式冲击。任何阶段的早期和后期修复阶段炎症反应模型进行了探讨。版权2001 Wiley-Liss公司。

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