Downregulation of connective tissue growth factor by LPS/IFN-γ-induced nitric oxide is reversed by aristolochic acid treatment in glomerular mesangial cells via STAT-1α and NF-κB signaling.

doi:10.1016/j.cbi.2013.12.017

中山醫學大學機構典藏 CSMUIR > 醫學院 > 免疫學研究所 > 期刊論文 > Item 310902500/11733

jsp.display-item.identifier=請使用永久網址來引用或連結此文件: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11733

题名:	Downregulation of connective tissue growth factor by LPS/IFN-γ-induced nitric oxide is reversed by aristolochic acid treatment in glomerular mesangial cells via STAT-1α and NF-κB signaling.
作者:	Tsai, KD W, Chen SH, Wang YW, Hsiao JY, Chi HY, Wu YJ, Lee HY, Wong MJ, Tseng Lin, TH
贡献者:	中山醫學大學
关键词:	Nitric oxide;Aristolochic acid;Connective tissue growth factor;Glomerular mesangial cells;STAT-1α;NF-κB
日期:	2014
上传时间:	2015-07-28T09:02:54Z (UTC)
ISSN:	0009-2797
摘要:	Aristolochic acid (AA) is a common cause of Chinese herb nephropathy. The mechanisms involved in the pathogenesis of AA nephropathy (AAN) are intricate. One well-documented effect of AA in the kidney is its pro-fibrotic activity. Nitric oxide (NO), a messenger gas generated from l-arginine, is the product of nitric oxide synthase (NOS). NO is involved in renal hemodynamics and exerts cytoprotective effects against renal injury. In the present study, the role of NO in AAN was investigated in MES-13 cells, a glomerular mesangial cell line. NO endogenously generated by the induction of inducible nitric oxide synthase (iNOS) with lipopolysaccharide (LPS)/interferon-γ (IFN-γ) significantly downregulated connective tissue growth factor (CTGF) protein expression in MES-13 cells. AA significantly suppressed LPS/IFN-γ-induced NO production and reversed CTGF expression that was downregulated by LPS/IFN-γ. AA decreased iNOS gene and protein expressions in a concentration-dependent manner. AA caused declines in LPS/IFN-γ-induced signal transducer and activator of transcription-1α (STAT-1α) phosphorylation and interferon response factor-1 (IRF-1) mRNA expression. Furthermore, AA attenuated IκB phosphorylation and reduced NF-κB translocation to the nuclear fraction. Taken together, our data indicate that AA reversed the CTGF expression inhibited by LPS/IFN-γ treatment via suppression of NO and iNOS expressions in MES-13 cells through inhibition of the JAK/STAT-1α and NF-κB signaling pathways. NO potentially exerts antifibrotic activity by down regulation of CTGF in MES-13 cells and inhibition of the iNOS gene by AA might partially account for the fibrotic effects of AA in nephropathy.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11733 http://dx.doi.org/10.1016/j.cbi.2013.12.017
關聯:	Chem Biol Interact. 2014 Mar 5;210:86-95.
显示于类别:	[免疫學研究所] 期刊論文

文件中的档案:

档案	描述	大小	格式	浏览次数
index.html	期刊論文	0Kb	HTML	476	检视/开启

检视Licence

在CSMUIR中所有的数据项都受到原著作权保护.

TAIR相关文章

数据加载中.....