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首页> 外文期刊>American Journal of Physiology >Interleukin-10-mediated inhibition of free radical generation in macrophages.
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Interleukin-10-mediated inhibition of free radical generation in macrophages.

机译：白介素10介导的巨噬细胞自由基产生的抑制。

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摘要

Interleukin-10 (IL-10) is a pleiotropic cytokine that controls inflammatory processes by suppressing the production of proinflammatory cytokines that are known to be transcriptionally regulated by nuclear factor-kappaB (NF-kappaB). Although still controversial, IL-10 has been shown to inhibit NF-kappaB activation through a process that involves proteolytic degradation of inhibitory subunit IkappaB-alpha. What is not known, however, is the mechanism by which IL-10 exerts its effect on IkappaB-alpha degradation. The present study investigates the possible role of reactive oxygen species (ROS) and their inhibition by IL-10 in NF-kappaB activation and IkappaB-alpha degradation in macrophages. Treatment of the cells with lipopolysaccharide (LPS) caused activation of NF-kappaB and rapid proteolysis of IkappaB-alpha as determined by the electrophoretic mobility shift assay, gene transfection, and Western blot. IL-10 pretreatment inhibited both NF-kappaB activation and IkappaB-alpha degradation. Both of these processes were also inhibited by ROS scavengers, catalase (H(2)O(2) scavenger), and sodium formate (.OH scavenger) but were minimally affected by superoxide dismutase (O scavenger). These results suggests that.OH radicals, formed by an H(2)O(2)-dependent, metal-catalyzed Fenton reaction, play a major role in this process. Electron spin resonance studies confirmed the formation of.OH radicals in LPS-treated cells. Addition of IL-10 inhibited both IkappaB-alpha degradation and generation of.OH radicals in response to LPS stimulation. These results demonstrate, for the first time, direct evidence for the role of IL-10 in ROS-dependent NF-kappaB activation.
机译：白介素10（IL-10）是一种多效性细胞因子，可通过抑制促炎细胞因子的产生来控制炎症过程，促炎细胞因子的产生已知由核因子-κB（NF-kappaB）转录调控。尽管仍存在争议，但IL-10已显示出通过涉及抑制性亚基IkappaB-α蛋白水解降解的过程抑制NF-κB活化。但是，IL-10对IkappaB-α降解发挥作用的机制尚不清楚。本研究调查了活性氧（ROS）的可能作用以及IL-10对巨噬细胞中NF-κB活化和Ikappa-α降解的抑制作用。脂多糖（LPS）处理细胞会导致NF-κB的活化和IkappaB-α的快速蛋白水解，这是通过电泳迁移率变动分析，基因转染和Western印迹法确定的。 IL-10预处理同时抑制NF-κB活化和IkappaB-α降解。这两个过程也都被ROS清除剂，过氧化氢酶（H（2）O（2）清除剂）和甲酸钠（.OH清除剂）抑制，但受超氧化物歧化酶（O清除剂）的影响最小。这些结果表明，由H（2）O（2）依赖，金属催化的Fenton反应形成的OH自由基在此过程中起主要作用。电子自旋共振研究证实了LPS处理的细胞中OH自由基的形成。 IL-10的添加可抑制IkappaB-α降解以及响应LPS刺激而产生的OH自由基。这些结果首次证明了IL-10在ROS依赖性NF-κB激活中的作用的直接证据。

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