中国药理学通报2018，Vol.34Issue(1)：60-67,8.DOI:10.3969/j.issn.1001-1978.2018.01.014
积雪草酸通过调节TLR4和PPAR-γ活性抑制内毒素诱导的血管平滑肌细胞炎症反应
Asiatic acid inhibits LPS-induced inflammatory response via Cardiology, regulating TLR4 and PPAR-γin VSMCs
摘要
Abstract
Aim To observe whether asiatic acid ( AA) can inhibit lipopolysaccharide ( LPS )-induced inflammatory response in VSMCs , and explore its mechanism of action .Methods The VSMCs isolated from aorta of SD rats were primarily cultured . The effect of AA on the cell viability of VSMCs was meas-ured by MTT assay .The protein and mRNA expression of IL-6, MCP-1, and TNF-α, were measured by ELISA assay and real-time PCR, respectively.The protein and mRNA of TLR4 and PPAR-γwere meas-ured by Western blot and real-time PCR, respectively . Results AA exhibited no effect on cellular viability between the concentration from 0 to 30 μmol · L-1 . After treating VSMCs with LPS (500μg· L-1 ) for 6h or 24 h, the protein and mRNA expression of IL-6, MCP-1, TNF-α, and TLR4 significantly increased ( P<0.05 );and on the contrary , the activity of PPAR-γwas significantly reduced ( P<0.05 ) .Treatment with AA (10, 20, 30 μmol· L-1 ) could concentration-de-pendently inhibit LPS-induced protein and mRNA ex-pression of IL-6, MCP-1, TNF-α.AA could also re-duce LPS-induced protein and mRNA expression of TLR4, and pretreatment of the cells with TLR4-siRNA could reduce LPS-induced inflammation . Moreover , treatment with AA could up-regulate the mRNA and protein expression of PPAR-γin VSMCs; however , GW9662 , a PPAR-γantagonist , partially attenuated AA' s anti-inflammatory effect .Conclusion AA can significantly inhibit LPS-induced mRNA and protein expression of IL-6, MCP-1, TNF-α, in VSMCs, which is partially dependent on suppressing TLR 4 and up-regulating PPAR-γ.关键词
积雪草酸/血管平滑肌细胞/内毒素/Toll受体4/过氧化物酶增殖物激活受体-γ/炎症反应Key words
asiatic acid/lipopolysaccharide/Toll-like receptor 4/peroxisome proliferators -activated recep-tors-γ/inflammatory response分类
医药卫生引用本文复制引用
孟哲,李海禹,刘宇宙,陶海龙,李凌..积雪草酸通过调节TLR4和PPAR-γ活性抑制内毒素诱导的血管平滑肌细胞炎症反应[J].中国药理学通报,2018,34(1):60-67,8.基金项目
河南省卫生厅科技攻关项目(No201403051) （No201403051）
