Tetramethoxy hydroxyflavone p7F downregulates inflammatory mediators via the inhibition of nuclear factor κB

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Title
Tetramethoxy hydroxyflavone p7F downregulates inflammatory mediators via the inhibition of nuclear factor κB
Author(s)
Hee Gu Lee; Hyoson Kim; Won Keun Oh; Kyung Ae Yu; Yong Kyung Choe; Jong Seog Ahn; D S Kim; S H Kim; C A Dinarello; K Kim; Do Young Yoon
Bibliographic Citation
Annals of New York Academy of Sciences, vol. 1030, pp. 554-567
Publication Year
2004
Abstract
Artemisia has been traditionally used in Korean herbal medicine to clear damp heat and to treat uteritis and jaundice. Flavonoids isolated from Artemisia are also known to possess anti-inflammatory activities. In this study, 5,6,3′,5′-tetramethoxy 7,4′-hydroxyflavone (p7F) was isolated from Artemisia absinthium. We examined in vitro and in vivo regulatory functions of p7F on the production of nitric oxide (NO), prostaglandin E2 (PGE2), and tumor necrosis factor-α (TNF-α) as well as the expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and collagen-induced arthritis. p7F inhibited the expression or production of proinflammatory mediators such as COX-2/PGE2 and iNOS/NO in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. p7F also suppressed the serum level of TNF-α in mice treated with collagen and inhibited nuclear factor-κB (NF-κB) activation as well as NF-κB promoter activity in RAW 264.7 cells stimulated with LPS. This compound directly inhibited the intracellular accumulation of reactive oxygen species in hydrogen peroxide-stimulated RAW 264.7 cells. p7F has antioxidant activity and inhibits NF-κB activation. Taken together, these results suggest that p7F can be clinically applied to the treatment of inflammatory diseases.
Keyword
flavonoidinflammationnitric oxidenuclear factor-κBreactive oxygen species
ISSN
0077-8923
Publisher
Wiley
DOI
http://dx.doi.org/10.1196/annals.1329.065
Type
Article
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Ochang Branch Institute > Anticancer Agent Research Center > 1. Journal Articles
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