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Suppression of lipopolysaccharide-induced expression of inducible nitric oxide synthase by brazilin in RAW 264.7 macrophage cells

Title
Suppression of lipopolysaccharide-induced expression of inducible nitric oxide synthase by brazilin in RAW 264.7 macrophage cells
Authors
Bae I.-K.Min H.-Y.Han A.-R.Seo E.-K.Sang K.L.
Ewha Authors
이상국서은경한아름
SCOPUS Author ID
이상국scopus; 서은경scopus; 한아름scopusscopus
Issue Date
2005
Journal Title
European Journal of Pharmacology
ISSN
0014-2999JCR Link
Citation
European Journal of Pharmacology vol. 513, no. 3, pp. 237 - 242
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Brazilin (7,11b-dihydrobenz[b]indeno[1,2-d]pyran-3,6a,9,10 (6H)-tetrol) isolated from Caesalpinia sappan has been known as a natural red pigment. Many studies suggest that inducible isoform of nitric oxide synthase (NOS) plays an important role in inflammation and carcinogenesis. On this line, we evaluated the inhibitory effect of brazilin on nitric oxide (NO) production and investigated its mechanism of action. As a result, brazilin exhibited the inhibitory effect on lipopolysaccharide (LPS)-stimulated NO production in a dose-dependent manner (IC50 = 24.3 μM). In addition, brazilin suppressed LPS-induced iNOS protein and mRNA expression in RAW 264.7 macrophage cells, indicating that the inhibitory activity of brazilin possibly involved in the regulation of iNOS expression. To further investigate the mechanism responsible for the suppression of iNOS gene expression by brazilin, the effect of brazilin on LPS-induced transcription factors nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) activation was examined. The DNA binding activity of NF-κB and AP-1 stimulated LPS was inhibited by treatment of brazilin in a dose-dependent manner, suggesting that brazilin-mediated inhibition of NO production might be associated with the regulation of transcription factors NF-κB and AP-1. Taken together, these findings suggest that the suppressive effect of iNOS gene expression by brazilin might provide one possible mechanism for its anti-inflammatory and cancer chemopreventive activity. © 2005 Elsevier B.V. All rights reserved.
DOI
10.1016/j.ejphar.2005.03.011
Appears in Collections:
약학대학 > 약학과 > Journal papers
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