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TLR4在 LPS 诱导的结肠炎症恢复中的作用

李旺林 刘梦鳌 曹杰 杨平 郑晓彬 董博业 卢嘉宝

中国病理生理杂志2017,Vol.33Issue(2):336-343,8.
中国病理生理杂志2017,Vol.33Issue(2):336-343,8.DOI:10.3969/j.issn.1000-4718.2017.02.023

TLR4在 LPS 诱导的结肠炎症恢复中的作用

Role of TLR4 in process of colonic inflammation recovery induced by LPS

李旺林 1刘梦鳌 1曹杰 1杨平 1郑晓彬 1董博业 1卢嘉宝1

作者信息

  • 1. 广州医科大学附属广州市第一人民医院胃肠外科,广东广州510180
  • 折叠

摘要

Abstract

AIM: To study the roles of Toll-like receptor 4 ( TLR4 ) and TLR4 activator lipopolysaccharide ( LPS) in colonic inflammation recovery .METHODS:Normal intestinal epithelial cells were cultured with LPS in vitro. The subgroups of the intestinal epithelial cells with differential expression of TLR 4 ( low, normal and high ) were construc-ted by the technique of lentivirus transfection .The cells with normal and high expression of TLR 4 were induced by LPS for 0 h, 2 h and 4 h.Inflammatory cytokines TNF-α, IL-6 and IL-8 in the culture supernatant were detected by ELISA .The mRNA levels of TNF-α, IL-6, IL-8, IL-10 and IL-1βwere detected by qPCR .The cell mobility was also monitored by wound healing assay .RESULTS:The protein expression of TLR 4 was significantly higher after LPS treatment than that in control groups of both cells with TLR4 normal and high expression (P<0.05).The inflammatory cytokines TNF-α, IL-6, IL-8 and IL-1βat mRNA and protein levels were also significantly increased after LPS treatment compared with control group (P<0.05).The protein levels of TNF-α, IL-6 and IL-8 between the 2 groups were also different with statistical sig-nificance ( P<0.05 ) .Higher mobility was observed in the cells with TLR 4 high expression compared to control cells . CONCLUSION:LPS induction might play a role in the activation of TLR 4-mediated inflammatory pathways by up-regula-ting the expression of inflammatory cytokines at both transcriptional and translational levels .

关键词

炎症性肠病/Toll样受体4/脂多糖

Key words

Inflammatory bowel disease/Toll-like receptor 4/Lipopolysaccharide

分类

医药卫生

引用本文复制引用

李旺林,刘梦鳌,曹杰,杨平,郑晓彬,董博业,卢嘉宝..TLR4在 LPS 诱导的结肠炎症恢复中的作用[J].中国病理生理杂志,2017,33(2):336-343,8.

基金项目

广州市科技计划(No.2014Y2-00074);广东省自然科学基金资助项目 ()

中国病理生理杂志

OA北大核心CSCDCSTPCD

1000-4718

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