Inhibition of intracerebroventricular injection stress-induced plasma corticosterone levels by intracerebroventricularly administered compound K, a ginseng saponin metabolite, in mice.
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-->6)-beta-D-glucopyranosyl]-20(S)-protopanaxadiol), and ginsenoside Mc (IH-903, 20-O-[alpha-L-arabinofuranosyl (1-->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.
Kim
Do-Hoon
DH
Department of Psychiatry, College of Medicine, Institute of Natural Medicine, Hallym University, Chunchon, Kangwon-Do, Korea.
Jung
Jun-Sub
JS
Moon
Yoo-Sun
YS
Sung
Jong-Hwan
JH
Suh
Hong-Won
HW
Kim
Yung-Hi
YH
Song
Dong-Keun
DK
D000818:Animals; D003345:Corticosterone / Q000037:antagonists & inhibitors / Q000097:blood*; D036145:Ginsenosides / Q000008:administration & dosage* / Q000737:chemistry / Q000378:metabolism; D007276:Injections, Intraventricular; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D005894:Panax / Q000378:metabolism; D012503:Saponins / Q000008:administration & dosage* / Q000737:chemistry / Q000378:metabolism; D013312:Stress, Physiological / Q000097:blood* / Q000188:drug therapy
D003345:Corticosterone; D036145:Ginsenosides; D012503:Saponins; C112772:ginsenoside compound K