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首页> 外文期刊>Biochemical Pharmacology >Ginsenoside Rd ameliorates colitis by inducing p62-driven mitophagy-mediated NLRP3 inflammasome inactivation in mice
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Ginsenoside Rd ameliorates colitis by inducing p62-driven mitophagy-mediated NLRP3 inflammasome inactivation in mice

机译：人参皂甙RD通过诱导小鼠P62驱动的介导的NLRP3炎症体灭活来改善结肠炎

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摘要

Previous studies reported that Ginsenoside Rd (Rd) had anti-inflammatory and anti-cancer effects. However, the molecular mechanism underlying the inhibition effect of Rd on colitis in mice hasn’t been clarified clearly. Here, in our study, we detected the effects of Rd on dextran sulfate sodium (DSS)-induced murine colitis, and found that oral administration of Rd dose-dependently alleviated DSS-induced body weight loss, colon length shortening and colonic pathological damage with lower myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) activities and higher glutathione level. In addition, the production of pro-inflammatory cytokines (IL-1β, TNF-a and IL-6) in both serum and colonic tissues were significantly down-regulated by Rd administration. The activation of NLRP3 inflammasome was also suppressed in Rd-treated group, resulting in reduced caspase-1 production and IL-1β secretion. In vitro, Rd remarkably inhibited NLRP3 inflammasome activation which was mostly dependent on the mitochondrial translocation of p62 and mitophagy. Importantly, Rd-driven inhibition of the NLRP3 inflammasome was significantly blocked by various autophagy inhibitors. Furthermore, upregulation of AMPK/ULK1 signaling pathway accounted for Rd-induced autophagy, which was also seen in vivo. In conclusion, our results demonstrated the function of Rd on the inhibition NLRP3 inflammasome and its potential application for the treatment of NLRP3-associated diseases.
机译：以前的研究报告说，人参皂苷Rd（RD）具有抗炎和抗癌作用。然而，尚未明确阐明RD抑制作用抑制作用对小鼠结肠炎的分子机制。在这里，在我们的研究中，我们检测到Rd对葡聚糖硫酸钠钠（DSS）诱导的鼠结肠炎的影响，并发现口服施用RD剂量依赖性缓解DSS诱导的体重损失，结肠长度缩短和结肠病理损伤降低髓过氧化物酶（MPO）和诱导型一氧化氮合酶（INOS）活性和更高的谷胱甘肽水平。此外，通过RD施用显着下调血清和结肠组织中的促炎细胞因子（IL-1β，TNF-A和IL-6）的产生。在RD处理基团中也抑制了NLRP3炎性的活化，导致Caspase-1产生降低的生产和IL-1β分泌。体外，RD显着抑制NLRP3炎症体活化，其主要取决于P62和MITOCHAGY的线粒体易位。重要的是，通过各种自噬抑制剂显着阻断NLRP3炎性组的RD驱动抑制。此外，AMPK / ULK1信号传导途径的上调占RD诱导的自噬，其在体内也看到。总之，我们的结果证明了RD对抑制NLRP3炎性的功能及其治疗NLRP3相关疾病的潜在应用。

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  • 来源
    《Biochemical Pharmacology》 |2018年第2018期|共14页
  • 作者

    Chao Liu; Jianing Wang; Yan Yang; Xiuting Liu; Yubing Zhu; Jianjun Zou; Sishi Peng; Thi Ha Le; Yu Chen; Shuli Zhao; Bangshun He; Qiongyu Mi; Xu Zhang; Qianming Du;

  • 作者单位

    Department of Pharmacy Nanjing First Hospital Nanjing Medical University;

    Neurobiology Laboratory Jiangsu Center for Drug Screening China Pharmaceutical University;

    Department of Pharmacy The Third People's Hospital of Chengdu &

    Affiliated Hospital of Southwest;

    Department of Clinical Pharmacy School of Basic Medicine &

    Clinical Pharmacy China Pharmaceutical;

    Department of Pharmacy Nanjing First Hospital Nanjing Medical University;

    Department of Pharmacy Nanjing First Hospital Nanjing Medical University;

    Department of Clinical Pharmacy School of Basic Medicine &

    Clinical Pharmacy China Pharmaceutical;

    Department of Pharmacy Nanjing First Hospital Nanjing Medical University;

    Department of Pharmacy Nanjing First Hospital Nanjing Medical University;

    General Clinical Research Center Nanjing First Hospital Nanjing Medical University;

    General Clinical Research Center Nanjing First Hospital Nanjing Medical University;

    General Clinical Research Center Nanjing First Hospital Nanjing Medical University;

    Department of Medicine The First People’s Hospital of Chengdu &

    Affiliated Hospital of Chengdu;

    Department of Clinical Pharmacy School of Basic Medicine &

    Clinical Pharmacy China Pharmaceutical;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 药理学;
  • 关键词

    Ulcerative colitis; Inflammation; Ginsenoside Rd; NLRP3 Inflammasome; P62;

    机译：溃疡性结肠炎;炎症;人参皂苷Rd;NLRP3炎症;P62;

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