Mechanism of CINC-1 production from gastric epithelial cells stimulated with TNF-α

被引：0
|
作者：
Handa, O [1 ]
Naito, Y [1 ]
Takagi, T [1 ]
Ueda, M [1 ]
Ishikawa, T [1 ]
Imamoto, E [1 ]
Tomatsuri, N [1 ]
Uchiyama, K [1 ]
Shimozawa, M [1 ]
Katada, K [1 ]
Ueda, T [1 ]
Kokura, S [1 ]
Ichikawa, H [1 ]
Yoshida, N [1 ]
Yoshikawa, T [1 ]
Gediminas, C [1 ]
Kvietys, PR [1 ]
机构：
[1] Lawson Hlth Res Inst, Vasc Cell Biol Inflammat Program, London, ON, Canada
来源：
XI BIENNIAL MEETING OF THE SOCIETY FOR FREE RADICAL RESEARCH INTERNATIONAL | 2002年
关键词：
D O I：
暂无
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
CINC-1 has been suggested to play a role as a mediator of inflammatory reactions with neutrophil infiltration in rats. In this study, e investigate the mechanism of CINC-1 production from rat gastric mucosal cell (RGM-1) in response to TNF-alpha stimulation in vitro. TNF-alpha stimulation results in, 1) up-regulation of CINC-1 mRNA and protein, 2) NF-kappaB p65 activation, and 3) increase in cH(2)DCF-DA oxidation. These changes were reversed by several inhibitors against NF-kappaB activation, endogenous reactive oxygen production. In conclusion, TNF-alpha-induced CINC-1 production from RGM-1 cells depends on NF-kappaB and oxidative stress.
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页码：347 / 350
页数：4
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