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首页> 外文期刊>International immunopharmacology >Quercetin protects mouse liver against CCl4-induced inflammation by the TLR2/4 and MAPK/NF-kappa B pathway
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Quercetin protects mouse liver against CCl4-induced inflammation by the TLR2/4 and MAPK/NF-kappa B pathway

机译：槲皮素通过TLR2 / 4和MAPK / NF-Kappa B途径保护小鼠肝脏对抗CCL4诱导的炎症

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摘要

Quercetin (QE), a natural flavonoid, has many medical beneficial effects. However, its protective effects against carbon tetrachloride (CCl4) induced injury in liver have not been clarified. The aim of the present study is to illustrate the effects of QE on hepatic oxidative injury and inflammation in mice exposed to CCl4. ICR (Institute of Cancer Research) mice were exposed to CCl4 with or without QE co-administration for one week. Our results showed that QE administration significantly inhibited CCl4-induced liver injury. One of the potential mechanisms of QE action was decreasing the oxidative stress, which is consistent with decreasing of lipid peroxidation level and increasing the antioxidant enzyme activities in livers of mice. Furthermore, QE significantly decreased cytochrome P450 2E1 (CYP2E1) expression and production of pro-inflammatory markers such as inducible nitric oxide synthase (iNOS), interleukin-1 beta (IL-1 beta), cyclooxygenase-2 (COX-2) and nitric oxide (NO) in livers of CCl4-treated mouse. In the process of exploring the underlying mechanisms of QE action, we found that QE significantly inhibited the Toll-like receptor 2 (TLR2) and the Toll-like receptor 4 (TLR4) activation and mitogen-activated protein kinase (MAPK) phosphorylation, which in turn inactivated NF-kappa B and the inflammatory cytokines in livers of the CCl4-treated mice. In conclusion, these results suggested that the inhibition of CCl4-induced inflammation by QE is due to its anti-oxidant activity and its ability to modulate the TLR2/TLR4 and MAPK/NF-kappa B signaling pathway. (C) 2015 Elsevier B.V. All rights reserved.
机译：槲皮素（QE），一种天然的黄酮类化合物，具有许多医疗有益效果。然而，它尚未澄清其对四氯化碳（CCL4）诱导的肝脏损伤的保护作用。本研究的目的是说明QE对暴露于CCL4的小鼠肝氧化损伤和炎症的影响。 ICR（癌症研究所）小鼠接触到CCL4，没有QE共同给药一周。我们的研究结果表明，QE管理显着抑制CCL4诱导的肝损伤。 QE作用的潜在机制之一正在降低氧化应激，这与脂质过氧化水平的降低一致，并增加小鼠肝脏中的抗氧化酶活性。此外，QE显着降低细胞色素P450 2E1（CYP2E1）表达和生产促炎症标志物，例如诱导型一氧化氮合酶（InOS），白细胞介素-1β（IL-1β），环氧氧酶-2（COX-2）和硝酸氢在CCl4处理的小鼠的肝脏中氧化物（NO）。在探索QE动作的潜在机制的过程中，我们发现QE显着抑制了Toll样受体2（TLR2）和Toll样受体4（TLR4）活化和丝裂剂活化的蛋白激酶（MAPK）磷酸化，其反过来灭活的NF-Kappa B和CCL4处理的小鼠肝脏中的炎性细胞因子。总之，这些结果表明，QE抑制CCL4诱导的炎症是由于其抗氧化活性及其调节TLR2 / TLR4和MAPK / NF-Kappa B B信号通路的能力。 （c）2015 Elsevier B.v.保留所有权利。

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  • 来源
    《International immunopharmacology》 |2015年第1期|共9页
  • 作者

    Ma Jie-Qiong; Li Zhang; Xie Wan-Ru; Liu Chan-Min; Liu Si-Si;

  • 作者单位

    Sichuan Univ Sci &

    Engn Sch Chem &

    Pharmaceut Engn Zigong City 643000 Sichuan Provinc Peoples R;

    Sichuan Univ Sci &

    Engn Sch Chem &

    Pharmaceut Engn Zigong City 643000 Sichuan Provinc Peoples R;

    Sichuan Univ Sci &

    Engn Sch Chem &

    Pharmaceut Engn Zigong City 643000 Sichuan Provinc Peoples R;

    Jiangsu Normal Univ Sch Life Sci Xuzhou 221116 Jiangsu Peoples R China;

    Jiangsu Normal Univ Sch Life Sci Xuzhou 221116 Jiangsu Peoples R China;

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

    Quercetin; CCl4; Inflammation; TLR2/4; MAPK; Liver;

    机译：槲皮素;CCL4;炎症;TLR2 / 4;MAPK;肝脏;

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