Pharmacokinetic study of lancemaside A in mice and anti-inflammatory effect of its metabolite, echinocystic acid

To understand the anti-inflammatory effect of lancemaside A isolated from Codonopsis lanceolata Trautv. (family Campanulaceae), which ameliorates TNBS-induced colitis [1], we orally administered lancemaside A to mice and performed its pharmacokinetic study in mice by LC-MS/MS. Orally administered lancemaside A was metabolized to echinocystic acid via lancemaside X by intestinal microflora in mice by intestinal microflora and/or intestinal tissues and then absorbed it into the blood. Echinocystic acid also down-regulated inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as inflammatory mediators, NO and PGE2 in LPS-stimulated peritoneal macrophages. Orally and intraperitoneally administered echinocystic acid suppressed the production of pro-inflammatory cytokines, TNF-α and IL-1β, in LPS-injected mice. These results suggest that orally administered lancemaside A may be metabolized to echinocystic acid by intestinal microflora, and echinocystic acid be absorbed into the blood and shall express anti-inflammatory effects.

Acknowledgements: Financially supported by a grant (09172 KFDA 996) from Korean Food and Drug Administration (2009).

References: 1. Joh, E.H. et al. (2010) Int J Colorectal Dis. 25:545–551.