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Western blotting for ginseng saponins, ginsenosides using anti-ginsenoside Rb1 monoclonal antibody.

Ginsenosides separated by silica gel TLC were blotted to a polyvinylidene difluoride (PVDF) membrane which was treated with a NaIO4 solution followed by bovine serum albumine (BSA), resulting in a ginsenoside-BSA conjugate on a PVDF membrane. The blotted bands were stained with monoclonal antibody (MAb). The newly established Western blotting method was used for the determination of ginsenosides and their distribution in various Panax species.

Antibodies, Monoclonal↗

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.

Animals↗

Transformation of ginsenosides Rb2 and Rc from Panax ginseng by food microorganisms.

Protopanaxadiol ginsenosides Rb2 and Rc were transformed using cell-free extracts from various edible food microorganisms and then analyzed by TLC and HPLC. Rb2 and Rc were transformed into compound K via Rd and F2 by Bifidobacterium sp. Int57 and Bifidobacterium sp. SJ32. Lactobacillus delbrueckii transformed Rb2 and Rc into ginsenoside Rh2. Bifidobacterium sp. SH5 transformed Rb2 and Rc into F2. Aspergillus niger transformed Rb2 into compound K via compound O and compound Y, whereas it transformed Rc into compound K via Mc. Taken together, these processes would allow a specific bioconversion process to obtain specific ginsenosides using an appropriate combination of ginsenoside substrates and specific microbial enzymes.

Aspergillus niger↗