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冬凌草甲素对LPS诱导Raw264.7巨噬细胞炎症反应的抑制作用

郐一贺 顾取良 邓慧君 亓翠玲 王丽京

广东药学院学报2017,Vol.33Issue(2):250-254,5.
广东药学院学报2017,Vol.33Issue(2):250-254,5.DOI:10.16809/j.cnki.2096-3653.2017022601

冬凌草甲素对LPS诱导Raw264.7巨噬细胞炎症反应的抑制作用

Inhibition of oridonin on LPS-induced inflammation response in Raw264.7 macrophages

郐一贺 1顾取良 1邓慧君 2亓翠玲 1王丽京1

作者信息

  • 1. 广东药科大学 基础学院,广东 广州510006
  • 2. 广东药科大学 健康学院,广东 广州510006
  • 折叠

摘要

Abstract

Objective To investigate the effect of oridonin on lipopolysaccharide (LPS)-induced inflammation response in Raw264.7 macrophage cell line.Methods The optimal concentration of oridonin on Raw264.7 macrophages was determined by CCK8 method.The inflammation models were established by LPS stimulation and divided into four groups including the normal control,the LPS group,the experimental group (oridonin pretreatment + LPS) and the positive control (dexamethasone pretreatment+LPS).The changes of TNF-α,IL-1β,IL-6,IL-10 and TLR4 mRNA levels were measured by real-time quantitative PCR.The expression of NF-κB p65 and phosphorylated p65 (p-p65) were detected by western blot.Results At the optimal concentration (10 μmol/L),oridonin pretreatment significantly inhibited the expression of TNF-α,IL-1β and IL-6 mRNA induced by LPS and increased the expression of IL-10 mRNA in Raw264.7 cells.Oridonin also inhibited the expression of TLR4 and activation of NF-κB translocation into nucleus.Conclusion Oridonin can inhibit the expression of proinflammatory cytokines induced by LPS and exert anti-inflammation immune mechanism through TLR4-NF-κB signaling pathway.

关键词

冬凌草甲素/Raw264.7巨噬细胞/Toll样受体4/NF-κB

Key words

oridonin/macrophages/Toll-like receptor 4/nuclear factor-κB

分类

医药卫生

引用本文复制引用

郐一贺,顾取良,邓慧君,亓翠玲,王丽京..冬凌草甲素对LPS诱导Raw264.7巨噬细胞炎症反应的抑制作用[J].广东药学院学报,2017,33(2):250-254,5.

基金项目

国家自然科学基金项目(31471290) (31471290)

广东省科技计划项目(2013B021800082) (2013B021800082)

广东药学院学报

OACSTPCD

1006-8783

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