Asiatic acid inhibits LPS-induced inflammatory response via Cardiology, regulating TLR4 and PPAR-γin VSMCs
10.3969/j.issn.1001-1978.2018.01.014
- VernacularTitle: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
- Author:
Zhe MENG
1
;
yu Hai LI
;
zhou Yu LIU
;
long Hai TAO
;
Ling LI
Author Information
1. 郑州大学第一附属医院心血管内科
- Keywords:
asiatic acid;
lipopolysaccharide;
Toll-like receptor 4;
peroxisome proliferators -activated recep-tors-γ;
inflammatory response
- From:
Chinese Pharmacological Bulletin
2018;34(1):60-67
- CountryChina
- Language:Chinese
-
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.
