期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 371, 期 3, 页码 361-365出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2008.04.054
关键词
tranilast; heme oxygenase-1; extracellular signal-regulated kinase-1/2; cyclooxygenase-2; inducible nitric oxide synthase; tumor necrosis factor-alpha; interleukin-1 beta; macrophage; inflammation
Tranilast (N-[3',4'-dimethoxycinnamonyl] anthranilic acid), an orally active anti-allergic drug, is reported to exert the anti-inflammatory effects, but the underlying mechanisms that could explain the antiinflammatory actions of tranilast remain largely unknown. Here, we found that tranilast induces heme oxygenase-1 (HO-1) expression through the extracellular signal-regulated kinase-1/2 (ERK1/2) pathway in RAW264.7 macrophages. Tranilast suppressed cyclooxygenase-2 (COX-2) and inducible nitric oxide (NO) synthase (iNOS) expression and thereby reduced COX-2-derived prostaglandin E-2 (PGE(2)) and iNOS-derived NO production in lipopolysaccharide (LPS)-stimulated macrophages. Similarly, tranilast diminished tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 P (IL-1 beta) production. Interestingly, the effects of tranilast on LPS-incluced PGE(2), NO, TNF-alpha, and IL-1 beta production were partially reversed by the HO-1 inhibitor tin protoporpoyrin, suggesting that tranilast-induced HO-1 expression is at least partly responsible for the resulting anti-inflammatory effects of the drug. Thus, HO-I expression via ERK1/2 activation may be at least one of the possible mechanisms explaining the anti-inflammatory actions of tranilast. (C) 2008 Published by Elsevier Inc.
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