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过氧亚硝酸盐可保护RAW 264.7巨噬细胞免受脂多糖/γ干扰素诱导的细胞死亡。

Peroxynitrite protects RAW 264.7 macrophage from Lipopolysaccharide/Interferon-gamma-induced cell death.

作者信息

Scivittaro V, Boggs S, Mohr S, Lapetina E G

机构信息

Molecular Cardiovascular Research Center, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, Ohio 44106, USA.

出版信息

Biochem Biophys Res Commun. 1997 Dec 8;241(1):37-42. doi: 10.1006/bbrc.1997.7709.

Abstract

Peroxynitrite, formed by the interaction of superoxide with nitric oxide, has previously been implicated mostly as a cytotoxic agent. In contrast, its physiological and, possibly, beneficial effects are largely unknown. We have previously shown [Journal of Biological Chemistry, 1997, 272, 7253] that RAW 264.7 macrophages can be selected to be resistant toward lipopolysaccharide (LPS)/interferon-gamma (IFN-gamma)-induced cytotoxicity. Resistant cells produced comparable amount of nitric oxide, but showed increased formation of superoxide, which might lead to increased production of peroxynitrite. We utilized this well characterized cell model to seek evidence that peroxynitrite might cause protection of RAW cells from cytokine toxicity. Exogenous peroxynitrite (30-50 microM), applied to RAW cells before cytokine stimulation, dramatically reduced LPS/IFN-gamma toxicity. Measurement of cell viability after overnight incubation with a mixture of LPS (10 microg/ml) and IFN-gamma (100 U/ml), showed that pretreatment with 40 microM peroxynitrite completely reverted LPS/IFN-gamma cytotoxicity. Differently, pretreatment of RAW cells with peroxynitrite (10-60 microM) did not prevent cytotoxicity induced by the nitric oxide-donors S-Nitroso-L-glutathione (0.2-1 mM), or spermine NONOate (0.2-2 mM), and by Actimomycin D (0.5-1 microg/ml), suggesting that the protective effect is specific for the LPS/IFN-gamma pathway. These results were confirmed through extensive controlled studies aimed to optimize cell exposure to peroxynitrite, and showed that peroxynitrite protects macrophages from cytokine-induced cytotoxicity.

摘要

过氧亚硝酸盐由超氧化物与一氧化氮相互作用形成,此前大多被认为是一种细胞毒性剂。相比之下,其生理作用以及可能的有益作用在很大程度上尚不明确。我们之前已经表明[《生物化学杂志》,1997年,第272卷,第7253页],RAW 264.7巨噬细胞可以被选择为对脂多糖(LPS)/干扰素-γ(IFN-γ)诱导的细胞毒性具有抗性。抗性细胞产生的一氧化氮量相当,但超氧化物的形成增加,这可能导致过氧亚硝酸盐的产生增加。我们利用这个特征明确的细胞模型来寻找证据,证明过氧亚硝酸盐可能会保护RAW细胞免受细胞因子毒性的影响。在细胞因子刺激之前将外源性过氧亚硝酸盐(30 - 50微摩尔)应用于RAW细胞,可显著降低LPS/IFN-γ毒性。用LPS(10微克/毫升)和IFN-γ(100单位/毫升)的混合物过夜孵育后测量细胞活力,结果表明用40微摩尔过氧亚硝酸盐预处理可完全逆转LPS/IFN-γ细胞毒性。不同的是,用10 - 60微摩尔过氧亚硝酸盐预处理RAW细胞并不能预防一氧化氮供体S-亚硝基-L-谷胱甘肽(0.2 - 1毫摩尔)、精胺亚硝酰基供体(0.2 - 2毫摩尔)以及放线菌素D(0.5 - 1微克/毫升)诱导的细胞毒性,这表明保护作用对LPS/IFN-γ途径具有特异性。这些结果通过旨在优化细胞与过氧亚硝酸盐接触的广泛对照研究得到了证实,结果表明过氧亚硝酸盐可保护巨噬细胞免受细胞因子诱导的细胞毒性。

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