The fungal metabolite, citrinin, inhibits lipopolysaccharide/interferon-γ-induced nitric oxide production in glomerular mesangial cells.

doi:10.1016/j.intimp.2010.09.017

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 310902500/11736

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题名:	The fungal metabolite, citrinin, inhibits lipopolysaccharide/interferon-γ-induced nitric oxide production in glomerular mesangial cells.
作者:	Liu, BH Chi, JY Hsiao, YW Tsai, KD Lee, YJ Lin, CC Hsu, SC Yang, SM Lin, TH
贡献者:	中山醫學大學
关键词:	Citrinin;Nitric oxide;iNOS;STAT-1α;NF-κB;MES-13 cells
日期:	2010
上传时间:	2015-07-28T09:08:09Z (UTC)
ISSN:	1567-5769
摘要:	The mycotoxin, citrinin (CTN), is a secondary metabolite of the fermented products of Monascus. The mycotoxin can either suppress or stimulate immune responses. In the present study, the immunomodulatory role of CTN in nitric oxide (NO) production, a proinflammatory mediator in the process of inflammation, was investigated. NO is well known as a mediator of immune responses. Overproduction of NO catalyzed by inducible nitric oxide synthase (iNOS) protects host cells against microbial invasion, while aberrant iNOS induction is associated with the pathophysiology of inflammatory events. Herein, we report that CTN significantly suppressed lipopolysaccharide (LPS)/interferon (IFN)-γ-induced NO production in MES-13 cells, a glomerular mesangial cell line. The percentage of NO reduction caused by CTN was far greater than that of the decline in cell viability. CTN decreased iNOS gene and protein expressions in concentration-dependent manners. CTN caused declines in LPS/IFN-γ-induced signal transducer and activator of transcription-1α (STAT-1α) phosphorylation. Furthermore, LPS/IFN-γ's induction of interferon response factor-1 (IRF-1) mRNA expression was inhibited by CTN. Moreover, CTN attenuated IκB-α phosphorylation and reduced NF-κB's translocation to the nuclear fraction. Taken together, our data indicated that CTN significantly suppressed NO and iNOS expressions in MES-13 cells via inhibition of the JAK/STAT-1α and NF-κB signaling pathways.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11736 http://dx.doi.org/10.1016/j.intimp.2010.09.017
關聯:	Int Immunopharmacol. 2010 Dec;10(12):1608-15.
显示于类别:	[免疫學研究所] 期刊論文

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