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Differential Effect of Bovine Serum Albumin on Ginsenoside Metabolite-Induced Inhibition of ${\alpha}3{\beta}4$ Nicotinic Acetylcholine Receptor Expressed in Xenopus Oocytes  

Lee, Jun-Ho (Research Laboratory for the Study of Ginseng Signal Transduction and Dept. of Physiology, College of Veterinary Medicine Konkuk University)
Jeong, Sang-Min (Research Laboratory for the Study of Ginseng Signal Transduction and Dept. of Physiology, College of Veterinary Medicine Konkuk University)
Lee, Byung-Hwan (Research Laboratory for the Study of Ginseng Signal Transduction and Dept. of Physiology, College of Veterinary Medicine Konkuk University)
Kim, Dong-Hyun (College of Pharmacy, KyungHee university)
Kim, Jong-Hoon (Research Laboratory for the Study of Ginseng Signal Transduction and Dept. of Physiology, College of Veterinary Medicine Konkuk University)
Kim, Jai-Il (Dept. of Life Science, Kwnangju Institute of Science and Technology)
Lee, Sang-Mok (Research Laboratory for the Study of Ginseng Signal Transduction and Dept. of Physiology, College of Veterinary Medicine Konkuk University)
Nah, Seung-Yeol (Research Laboratory for the Study of Ginseng Signal Transduction and Dept. of Physiology, College of Veterinary Medicine Konkuk University)
Publication Information
Archives of Pharmacal Research / v.26, no.10, 2003 , pp. 868-873 More about this Journal
Abstract
Ginsenosides, major active ingredients of Panax ginseng, that exhibit various pharmacological and physiological actions are transformed into compound K (CK) or M4 by intestinal microorganisms. CK is a metabolite derived from protopanaxadiol (PD) ginsenosides, whereas M4 is a metabolite derived from protopanaxatriol (PT) ginsenosides. Recent reports shows that ginsenosides might playa role as pro-drugs for these metabolites. In present study, we investigated the effect of bovine serum albumin (BSA), which is one of major binding proteins on various neurotransmitters, hormones, and other pharmacological agents, on ginsenoside $Rg_{2-}$, CK-, or M4-induced regulation of $\alpha3\beta4$ nicotinic acetylcholine (ACh) receptor channel activity expressed in Xenopus oocytes. In the absence of BSA, treatment of ACh elicited inward peak current ($I_{Ach}$) in oocytes expressing $\alpha3\beta4$ nicotinic ACh receptor. Co-treatment of ginsenoside $Rg_2$, CK, or M4 with ACh inhibited IAch in oocytes expressing $\alpha3\beta4$ nicotinic ACh receptor with reversible and dose-dependent manner. In the presence of 1% BSA, treatment of ACh still elicited $I_{Ach}$ in oocytes expressing $\alpha3\beta4$ nicotinic ACh receptor and co-treatment of ginsenoside $Rg_2$ or M4 but not CK with ACh inhibited $I_{Ach}$ in oocytes expressing $\alpha3\beta4$ nicotinic ACh receptor with reversible and dose-dependent manner. These results show that BSA interferes the action of CK rather than M4 on the inhibitory effect of $I_{Ach}$ in oocytes expressing $\alpha3\beta4$ nicotinic ACh receptor and further suggest that BSA exhibits a differential interaction on ginsenoside metabolites.
Keywords
Ginsenosides; Ginsenoside metabolites; CK; M4; Bovine serum albumin; Nicotinic acetylcholine receptor-gated ion channels; Xenopus oocytes;
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