基于NF-κB/IκBα信号通路探讨“通经利浊”针法对急性痛风性关节炎大鼠保护作用的机制研究

Protective mechanisms of“smoothen meridian and clear turbid dampness”acupuncture on rats with acute gouty arthritis through the NF-κB/IκBαsignaling pathway

目的本研究旨在探讨"通经利浊"针法对急性痛风性关节炎大鼠潜在的保护机制。方法模型组通过注射单钠尿酸盐(MSU)诱发大鼠急性痛风性关节炎。治疗组对大鼠进行"通经利浊"针法针刺治疗7 d,对照组口服秋水仙碱(1 mg/kg)给药7 d。结果实验结果表明,注射MSU可显著提高血清促炎细胞因子白介素-1β(IL-1β)、白介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的水平,应用"通经利浊"针法针刺治疗效果显著逆转(P<0.05);通过组织病理学检查,进一步明确了"通经利浊"针法的疗效,并对其保护作用机制进行了研究,结果表明"通经利浊"针法针刺抑制了MSU诱导的核因子κB(NF-κB)通路的激活。MSU诱发后,"通经利浊"针法针刺显著抑制了NF-κB p65的活化和蛋白κB-α(IκBα)的降解。结论"通经利浊"针法针刺可能通过抑制NF-κB/IκBα信号通路的激活从而起到对MSU诱发的急性痛风性关节炎的保护作用。

Objective The present study aimed to investigate the effects of"smoothen meridian and clear turbid dampness"(SMCTD)acupuncture on a model of acute gouty arthritis and explore its underlying mechanisms.Methods The model of acute gouty arthritis was induced in rats by monosodium urate(MSU)crystal injection.Next,the rats were treated with SMCTD acupuncture for 7 d or orally administered colchicine(1 mg/kg)for 7 d.Results MSU crystal injection induced a significant elevation in the concentrations of the serum proinflammatory cytokines interleukin(IL)-1β,IL-6 and tumor necrosis factor-α(TNF-α).Treatment with SMCTD acupuncture significantly reversed these MSU crystalinduced alterations(P<0.05).The therapeutic effects of SMCTD acupuncture were further examined by histopathological examination.Exploration of the underlying mechanisms of its actions revealed that SMCTD acupuncture inhibited the activation of the nuclear factorκB(NF-κB)pathway,which was induced by MSU crystal injection.SMCTD acupuncture also significantly inhibited the activation of NF-κB p65 and the degradation of proteinκB-α(IκBα)after the MSU crystal challenge.Conclusions Taken together,our findings demonstrate that SMCTD acupuncture has beneficial effects on MSU crystal-induced acute gouty arthritis,probably by inhibiting activation of the NF-κB/IκBαsignaling pathway.