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Niacin attenuates the production of pro-inflammatory cytokines in LPS-induced mouse alveolar macrophages by HCA2 dependent mechanisms

机译:烟酸通过HCA2依赖性机制减弱LPS诱导的小鼠肺泡巨噬细胞中促炎性细胞因子的产生

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Niacin has been reported to have potent anti-inflammatory effects in LPS-induced acute lung injury. However, the molecular mechanism of niacin has not been fully understood. The aim of the present study was to investigate the effects of niacin on the production of pro-inflammatory cytokines TNF-α, IL-6 and IL-1β in LPS-induced mouse alveolar macrophages and explore its underlying mechanism. Mouse alveolar macrophages were incubated in the presence or absence of various concentrations of niacin (1, 10, 100 μmol/l) 1 h before LPS (1 μg/ml) challenge. The results showed that niacin reduced the levels of TNF-α, IL-6 and IL-1β in LPS-challenged alveolar macrophages. Furthermore, NF-κB activation was inhibited by niacin through blocking the phosphorylation of NF-κB p65 and IκBα. In addition, silencing HCA2 abrogated the effect of niacin on the production of pro-inflammatory cytokines. These findings suggested that niacin attenuated the LPS-induced pro-inflammatory cytokines possibly mediated by HCA2 in LPS-challenged alveolar macrophages.
机译:据报道,烟酸在LPS诱导的急性肺损伤中具有有效的抗炎作用。但是,烟酸的分子机理尚未完全了解。本研究的目的是研究烟酸对LPS诱导的小鼠肺泡巨噬细胞促炎细胞因子TNF-α,IL-6和IL-1β产生的影响,并探讨其潜在机制。在LPS(1μg/ ml)攻击前1小时,在存在或不存在各种浓度烟酸(1、10、100μmol/ l)的情况下孵育小鼠肺泡巨噬细胞。结果表明,烟酸降低了LPS挑战的肺泡巨噬细胞中TNF-α,IL-6和IL-1β的水平。此外,烟酸通过阻断NF-κBp65和IκBα的磷酸化抑制了NF-κB的活化。另外,沉默HCA2消除了烟酸对促炎性细胞因子产生的影响。这些发现表明烟酸减弱了LPS挑战的肺泡巨噬细胞中可能由HCA2介导的LPS诱导的促炎细胞因子。

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