畜牧兽医学报 ›› 2019, Vol. 50 ›› Issue (2): 431-438.doi: 10.11843/j.issn.0366-6964.2019.02.022

• 临床兽医 • 上一篇    下一篇

α-倒捻子素通过抑制TLR4/NF-κB信号通路缓解LPS诱导IEC-6细胞的炎症

邹闻书1, 尹朋2, 金娜1, 高倩1, 刘凤华1*   

  1. 1. 北京农学院动物科学技术学院, 北京 102206;
    2. 中国科学院微生物研究所, 北京 100101
  • 收稿日期:2018-07-04 出版日期:2019-02-23 发布日期:2019-02-23
  • 通讯作者: 刘凤华,主要从事炎症的损伤修复与中兽药药理研究,E-mail:liufenghua1209@126.com
  • 作者简介:邹闻书(1992-),女,辽宁大连人,硕士生,主要从事炎症的损伤修复与中兽药药理研究,E-mail:zouwenshu080603@163.com
  • 基金资助:

    北京市科技计划课题(D171100002117002)

α-Mangostin Alleviates LPS-induced Inflammation by Inhibiting TLR4/NF-κB Signaling

ZOU Wenshu1, YIN Peng2, JIN Na1, GAO Qian1, LIU Fenghua1*   

  1. 1. Animal Science and Technology College, Beijing University of Agriculture, Beijing 102206, China;
    2. Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China
  • Received:2018-07-04 Online:2019-02-23 Published:2019-02-23

摘要:

旨在证明α-倒捻子素可以缓解脂多糖(LPS)诱导的IEC-6细胞的炎症并揭示其机制。笔者在体外培养的IEC-6细胞中构建LPS诱导的炎症模型,并通过流式细胞术、酶联免疫吸附测定(ELISA)、定量PCR(Q-PCR)、蛋白印迹(Western blot)的方法检测α-倒捻子素对LPS诱导的炎症是否有缓解作用。结果表明,5 μmol·L-1的α-倒捻子素预处理可以显著降低LPS诱导的前列腺素E2(PGE2)、白细胞介素-1β(IL-1β)、IL-6和肿瘤坏死因子-α(TNF-α)在IEC-6细胞中的分泌,以及环氧合酶2(COX-2)、IL-6、TNF-α、IL-1β mRNA的表达(P<0.05)。通过对炎症相关信号通路NF-κB的探究可见,α-倒捻子素能显著抑制Toll样受体4(TLR4)mRNA和NF-κB相关蛋白磷酸化IκBα(pIκBα)和磷酸化p65(pp65)的激活(P<0.05)。综上所述,α-倒捻子素可以通过TLR4/NF-κB信号通路来抑制LPS诱导的IEC-6细胞的炎症,并且可能是治疗炎症疾病的潜在选择。

Abstract:

The aim of this study was to prove that α-mangostin can alleviate the lipopolysaccharide (LPS)-induced inflammation of IEC-6 cells and reveal its mechanism. In this study, we constructed an LPS-induced inflammation model in IEC-6 cells in vitro, and examined whether LPS-induced inflammation was reduced by α-mangostin by means of the methods of rheumatology, ELISA, Q-PCR, and Western blot. The results showed that pretreatment with 5 μmol·L-1 α-mangostin significantly reduced the secretion of prostaglandin (PG) E2, interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α and the expression of COX-2, IL-6, TNF-α, IL-1β mRNA induced by LPS in IEC-6 cells (P<0.05). By investigating the inflammatory-related signaling pathway, NF-κB, we found that α-mangostin significantly inhibited the activation of TLR4 mRNA and NF-κB-related protein phosphorylated IκBα (pIκBα) and phosphorylated p65 (pp65) (P<0.05). In summary, α-mangostin can inhibit LPS-induced inflammation of IEC-6 cells through the TLR4/NF-κB signaling pathway and may be a potential treatment for inflammatory diseases.

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