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 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.