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Effects of major intestinal metabolites of ginsenosides, including compound K (IH-901, 20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol), compound Y (IH-902, 20-O-[alpha-L-arabinopyranosyl (1--&gt;6)-beta-D-glucopyranosyl]-20(S)-protopanaxadiol), and ginsenoside Mc (IH-903, 20-O-[alpha-L-arabinofuranosyl (1--&gt;6)-beta-D-glucopyranosyl]-20(S)-protopanaxadiol), on acute stress-induced plasma corticosterone levels were studied in mice. Intracerebroventricularly (i.c.v.) administered compound K (1 microg) 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.

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Inhibition of Intracerebroventricular Injection Stress-Induced Plasma Corticosterone Levels by Intracerebroventricularly Administered Compound K, a Ginseng Saponin Metabolite, in Mice