Inhibition of intracerebroventricular injection stress-induced plasma corticosterone levels by intracerebroventricularly administered compound K, a ginseng saponin metabolite, in mice

Abstract

Effects of major intestinal metabolites of ginsenosides, including compound K (IH-901, 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol), compound Y (IH-902, 20-O-[α-L-arabinopyranosyl (1→6)-β-D-glucopyranosyl]- 20(S)-protopanaxadiol), and ginsenoside Mc (IH-903, 20-O-[α-L- arabinofuranosyl (1→6)-β-D-glucopyranosyl]-20(S)-protopanaxadiol), on acute stress-induced plasma corticosterone levels were studied in mice. Intracerebroventricularly (i.c.v) administered compound K (1 μg) attenuated the i.c.v. injection stress-induced increase in plasma corticosterone level, and this inhibitory effect was not affected by co-administered N G-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor. Compound K administered intraperitoneally affected neither the i.c.v. injection stress- nor the immobilization stress-induced increase in plasma corticosterone levels. Compound K and ginsenoside Mc did not affect plasma corticosterone levels induced by the two stress modalities used in this study. © 2003 Pharmaceutical Society of Japan.