Inhibitory Effect of Ginsenoside Rb1 and Compound K on NO and Prostaglandin E2 Biosyntheses of RAW264.7 Cells Induced by Lipopolysaccharide

In this study, the antiinflammatory activities of ginsenoside Rb1, which is a main constituent of the root of Panax ginseng (Araliaceae), and of its metabolite compound K, as produced by human intestinal bacteria, on lipopolysaccharide (LPS)-induced RAW264.7 cells were investigated. Compound K poten...

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Bibliographic Details
Published in:Biological & pharmaceutical bulletin 2005, Vol.28(4), pp.652-656
Main Authors: Park, Eun-Kyung, Shin, Yong-Wook, Lee, Hae-Ung, Kim, Sung-Soo, Lee, Young-Churl, Lee, Boo-Yong, Kim, Dong-Hyun
Format: Article
Language:English
Subjects:
Animals
Anti-Inflammatory Agents - pharmacology
Cell Line
compound K
COX-2
Cyclooxygenase 2
Dinoprostone - biosynthesis
Gene Expression - drug effects
ginseng
Ginsenosides - pharmacokinetics
Ginsenosides - pharmacology
Ginsenosides - urine
inducible NO synthase (iNOS)
inflammation
Lipopolysaccharides - pharmacology
Male
NF-kappa B - metabolism
Nitric Oxide - biosynthesis
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type II
Prostaglandin-Endoperoxide Synthases - metabolism
Rats
Rats, Sprague-Dawley
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Summary:In this study, the antiinflammatory activities of ginsenoside Rb1, which is a main constituent of the root of Panax ginseng (Araliaceae), and of its metabolite compound K, as produced by human intestinal bacteria, on lipopolysaccharide (LPS)-induced RAW264.7 cells were investigated. Compound K potently inhibited the production of NO and prostaglandin E2 in LPS-induced RAW 264.7 cells, with IC50 values of 0.012 and 0.004 mM, respectively. Compound K also reduced the expression levels of the inducible NO synthase (iNOS) and COX-2 proteins and inhibited the activation of NF-kB, a nuclear transcription factor. Compound K inhibited the NO level produced by iNOS enzyme activity in a cell-free system, but did not inhibit COX-1 and 2 activities. When ginsenoside Rb1 was orally administered to rats, compound K, but not ginsenoside Rb1, were excreted in their urine. These findings suggest that ginsenoside Rb1 can be transformed to compound K by intestinal bacteria, and compound K may be effective against inflammation.
ISSN:0918-6158
1347-5215
DOI:10.1248/bpb.28.652