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首页> 外文期刊>Life sciences >The spin trap 5,5-dimethyl-1-pyrroline N-oxide inhibits lipopolysaccharide-induced inflammatory response in RAW 264.7 cells
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The spin trap 5,5-dimethyl-1-pyrroline N-oxide inhibits lipopolysaccharide-induced inflammatory response in RAW 264.7 cells

机译：自旋阱5,5-二甲基-1-吡咯啉N-氧化物抑制RAW 264.7细胞中脂多糖诱导的炎症反应

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Aim: Exposure of macrophages to lipopolysaccharide (LPS) induces oxidative and inflammatory stresses, which cause cell damage. Antioxidant and anti-inflammatory properties have been attributed to the nitrone spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO), commonly used in free radical analysis, but these aspects of DMPO have been little explored. In this study, we sought to establish the anti-inflammatory activity of DMPO, presumably by removing free radicals which otherwise help activate inflammatory response and damage cells. Main methods: RAW 264.7 macrophages were treated with LPS and/or DMPO for different time points, cell damage, production of inflammatory mediators, inducible nitric oxide synthase (iNOS) expression, NF-κB p65 activation, phosphorylation of MAPKs and Akt, and intracellular reactive oxygen species (ROS) were determined. Key findings: After cells were treated with LPS and/or DMPO for 24 h, DMPO reduced the LPS-induced inflammatory response as indicated by downregulated iNOS expression and production of inflammatory mediators. Accordingly, DMPO protected cells from LPS-induced cytotoxicity. In order to understand the mechanistic basis of these DMPO effects, the NF-κB p65 activation and the phosphorylation of MAPKs and Akt were examined. We found, by assaying cells treated with LPS and/or DMPO for 15-60 min, that DMPO inhibited the phosphorylation of MAPKs, Akt, and IκBα, and reduced the NF-κB p65 translocation. Furthermore, we demonstrated that DMPO inhibited LPS-induced ROS production. Significance: DMPO showed the anti-inflammatory activity and attenuated LPS-induced cell damage, most likely by reducing ROS production and thus preventing the subsequent inflammatory activation and damage.
机译：目的：巨噬细胞暴露于脂多糖（LPS）会引起氧化应激和炎症应激，从而引起细胞损伤。抗氧化剂和抗炎特性归因于自由基分析中常用的硝化氮自旋捕集阱5,5-二甲基-1-吡咯啉N-氧化物（DMPO），但对DMPO的这些方面却鲜有探索。在这项研究中，我们试图通过消除自由基来建立DMPO的抗炎活性，否则自由基会激活炎症反应并损害细胞。主要方法：用LPS和/或DMPO处理RAW 264.7巨噬细胞的时间点不同，细胞损伤，炎症介质产生，诱导型一氧化氮合酶（iNOS）表达，NF-κBp65活化，MAPK和Akt磷酸化以及细胞内测定了活性氧（ROS）。主要发现：用LPS和/或DMPO处理细胞24小时后，DMPO降低了LPS诱导的炎症反应，如iNOS表达下调和炎症介质产生所表明的。因此，DMPO保护细胞免受LPS诱导的细胞毒性。为了了解这些DMPO效应的机制基础，研究了NF-κBp65的活化以及MAPK和Akt的磷酸化。通过分析用LPS和/或DMPO处理15-60分钟的细胞，我们发现DMPO抑制了MAPK，Akt和IκBα的磷酸化，并减少了NF-κBp65的易位。此外，我们证明了DMPO抑制LPS诱导的ROS产生。意义：DMPO表现出抗炎活性，并减轻了LPS诱导的细胞损伤，很可能是通过减少ROS的产生，从而防止了随后的炎症活化和损伤。

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