We investigated the effects of ginsenosides, the active ingredient of ginseng, on neuronal or muscle-type nicotinic acetylcholine receptor channel activity expressed in Xenopus oocytes after injection of cRNA encoding bovine neuronal α3β4, α7 or human muscle αβδε subunits. Treatment with acetylcholine elicited an inward peak current (IACh) in oocytes expressing nicotinic acetylcholine receptor subtypes. Cotreatment with ginsenoside Rg2 and acetylcholine inhibited IACh in oocytes expressing with α3β4 or αβδε but not in oocytes expressing α7 nicotinic acetylcholine receptors. The inhibition of IACh by ginsenoside Rg2 was reversible and dose-dependent. The half-inhibitory concentrations (IC50) of ginsenoside Rg2 were 60.2±14.1 and 15.7±3.5 μM in oocytes expressing α3β4 and αβδε nicotinic acetylcholine receptors, respectively. The inhibition of IACh by ginsenoside Rg2 was voltage-independent and noncompetitive. Other ginsenosides besides ginsenoside Rg2 also inhibited IACh in oocytes expressing α3β4 or αβδε nicotinic acetylcholine receptors. The order of potency for the inhibition of IACh was ginsenoside Rg2>Rf>Re>Rg1>Rc>Rb2>Rb 1 in oocytes expressing α3β4 nicotinic acetylcholine receptors and was ginsenoside Rg2>Rf>Rg1>Re>Rb1>Rc>Rb 2 in oocytes expressing αβδε nicotinic acetylcholine receptors. These results indicate that ginsenosides might regulate nicotinic acetylcholine receptors in a differential manner and this regulation might be one of the pharmacological actions of Panax ginseng.
- Nicotinic acetylcholine receptor channel
- Xenopus oocyte
ASJC Scopus subject areas