Differential effect of bovine serum albumin on ginsenoside metabolite-induced inhibition of alpha3beta4 nicotinic acetylcholine receptor expressed in Xenopus oocytes.
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 play a 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 Rg2-, CK-, or M4-induced regulation of alpha3beta4 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 alpha3beta4 nicotinic ACh receptor. Co-treatment of ginsenoside Rg2, CK, or M4 with ACh inhibited I(ACh) in oocytes expressing (alpha3beta4 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 alpha3beta4 nicotinic ACh receptor and co-treatment of ginsenoside Rg2 or M4 but not CK with ACh inhibited I(ACh) in oocytes expressing alpha3beta4 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 alpha3beta4 nicotinic ACh receptor and further suggest that BSA exhibits a differential interaction on ginsenoside metabolites.
Lee
Jun-Ho
JH
Research Laboratory for the Study of Ginseng Signal Transduction, Dept. of Physiology, College of Veterinary Medicine, Konkuk University, Seoul 143-701, Korea.
Jeong
Sang Min
SM
Lee
Byung-Hwan
BH
Kim
Dong-Hyun
DH
Kim
Jong-Hoon
JH
Kim
Jai-Il
JI
Lee
Sang-Mok
SM
Nah
Seung-Yeol
SY
D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002417:Cattle; D018076:DNA, Complementary / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D036145:Ginsenosides / Q000737:chemistry / Q000378:metabolism / Q000494:pharmacology*; D015640:Ion Channel Gating / Q000187:drug effects; D009865:Oocytes / Q000187:drug effects* / Q000378:metabolism; D011978:Receptors, Nicotinic / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D012502:Sapogenins / Q000378:metabolism / Q000494:pharmacology; D012710:Serum Albumin, Bovine / Q000494:pharmacology*; D014315:Triterpenes / Q000378:metabolism / Q000494:pharmacology; D014982:Xenopus laevis
D000109:Acetylcholine; D018076:DNA, Complementary; D036145:Ginsenosides; D011978:Receptors, Nicotinic; D012502:Sapogenins; D012710:Serum Albumin, Bovine; D014315:Triterpenes; C403530:nicotinic receptor alpha3beta4; C081552:protopanaxatriol; C026474:ginsenoside Rg2; C112772:ginsenoside compound K