期刊
FEBS LETTERS
卷 582, 期 12, 页码 1643-1650出版社
WILEY
DOI: 10.1016/j.febslet.2008.04.016
关键词
dipyrithione; lipopolysaccharide; iNOS; COX-2; STAT1; endotoxic shock
Dipyrithione (PTS2) possesses anti-bacterial and anti-fungal activity. In the present study, we found that PTS2 dose-dependently inhibited the LPS-induced up-regulation of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein level in RAW264.7 cells. RT-PCR experiments showed that PTS2 suppressed LPS-induced iNOS but not COX-2 expression at the mRNA level. As expected, PTS2 prevented NO secretion in RAW264.7 cells. Furthermore, PTS2 administration significantly decreased LPS-induced mortality in mice. Mechanistically, PTS2 decreased expression and phosphorylation of STAT1, but did not interfere with the MAPK and NF-kappa B pathways. In conclusion, PTS2 protects mice against endotoxic shock and inhibits LPS-induced production of pro-inflammatory mediators, suggesting that PTS2 could play an anti-inflammatory role in response to LPS. (C) 2008 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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