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

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Effects of major intestinal metabolites of ginsenosides, including compound K (IH-901, 20-0-β-D-glucopyranosyl-20(S)-protopanaxadiol), compound Y (IH-902, 20-0-[α-L-arabinopyranosyl (1→6)-β-D-glucopyranosyl]- 20(S)-protopanaxadiol) , and ginsenoside Mc(IH-903, 20-0-[α-L-arabinopyranosyl (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 (1μg) 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.
公益社団法人日本薬学会の論文
2003-07-01