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Curcumin alleviates macrophage activation and lung inflammation induced by influenza virus infection through inhibiting the NF‐κB signaling pathway

机译:姜黄素通过抑制NF-κB信号通路减轻流感病毒感染引起的巨噬细胞活化和肺部炎症

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Abstract BackgroundInfluenza A viruses (IAV) result in severe public health problems with worldwide each year. Overresponse of immune system to IAV infection leads to complications, and ultimately causing morbidity and mortality. ObjectiveCurcumin has been reported to have anti-inflammatory ability. However, its molecular mechanism in immune responses remains unclear. MethodsWe detected the pro-inflammatory cytokine secretion and nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB)-related protein expression in human macrophages or mice infected by IAV with or without curcumin treatment. ResultsWe found that the IAV infection caused a dramatic enhancement of pro-inflammatory cytokine productions of human macrophages and mice immune cells. However, curcumin treatment after IAV infection downregulated these cytokines production in a dose-dependent manner. Moreover, the NF-κB has been activated in human macrophages after IAV infection, while administration of curcumin inhibited NF-κB signaling pathway via promoting the expression of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα), and inhibiting the translocation of p65 from cytoplasm to nucleus. ConclusionsIn summary, IAV infection could result in the inflammatory responses of immune cells, especially macrophages. Curcumin has the therapeutic potentials to relieve these inflammatory responses through inhibiting the NF-κB signaling pathway.
机译:摘要背景每年,甲型流感病毒(IAV)导致严重的公共卫生问题。免疫系统对IAV感染的过度反应会导致并发症,并最终导致发病率和死亡率。客观报道姜黄素具有抗炎能力。然而,其在免疫应答中的分子机制仍不清楚。方法我们检测了经或未经姜黄素治疗的IAV感染的人巨噬细胞或小鼠中活化B细胞(NF-κB)相关蛋白表达的促炎细胞因子分泌和核因子κ-轻链增强子。结果我们发现IAV感染引起人类巨噬细胞和小鼠免疫细胞促炎性细胞因子产生的显着增强。但是,IAV感染后姜黄素治疗以剂量依赖性方式下调了这些细胞因子的产生。此外,NF-κB在IAV感染后已在人类巨噬细胞中被激活,而姜黄素的给药通过促进B细胞抑制剂α(IκBα)中κ轻型多肽基因增强子的核因子表达而抑制了NF-κB信号通路,并抑制p65从细胞质到核的转运。结论总之,IAV感染可能导致免疫细胞,特别是巨噬细胞的炎症反应。姜黄素具有通过抑制NF-κB信号传导途径缓解这些炎症反应的治疗潜力。

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