title: Inhibitory effect of ginsenoside Rb1 and compound K on NO and prostaglandin E2 biosyntheses of RAW264.7 cells induced by lipopolysaccharide.
abstract: 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 IC(50) 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.
authors.affiliation: College of Pharmacy, Kyung Hee University, Seoul, Korea.
authors.forename: Eun-Kyung
authors.initials: EK
authors.lastname: Park
authors.forename: Yong-Wook
authors.initials: YW
authors.lastname: Shin
authors.forename: Hae-Ung
authors.initials: HU
authors.lastname: Lee
authors.forename: Sung-Soo
authors.initials: SS
authors.lastname: Kim
authors.forename: Young-Churl
authors.initials: YC
authors.lastname: Lee
authors.forename: Boo-Yong
authors.initials: BY
authors.lastname: Lee
authors.forename: Dong-Hyun
authors.initials: DH
authors.lastname: Kim
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002460:Cell Line; D051546:Cyclooxygenase 2; D015232:Dinoprostone / Q000096:biosynthesis*; D015870:Gene Expression / Q000187:drug effects; D036145:Ginsenosides / Q000493:pharmacokinetics / Q000494:pharmacology* / Q000652:urine; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000893:Anti-Inflammatory Agents; D051546:Cyclooxygenase 2; D015232:Dinoprostone; D036145:Ginsenosides; D008070:Lipopolysaccharides; D016328:NF-kappa B; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D011451:Prostaglandin-Endoperoxide Synthases; C442759:ginsenoside Rb1; C112772:ginsenoside compound K; C496318:Nos2 protein, rat