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Effects of Ginsenosides on GABAA Receptor Channels Expreaaed in Xenopus Oocytes
Se-EunChoi,SeokChoi,Jun-HoLee,PaulJ.Whiting,Sang-MokLee,Seoung-YeolNah 대한약학회 2003 Archives of Pharmacal Research Vol.26 No.1
Ginsenosides, major active ingredients of Panax ginseng, are known to regulate excitatory ligand-gated ion channel activity such as nicotinic acetylcholine and NMDA receptor channel activity. However, it is not known whether ginsenosides affect inhibitory ligand-gated ion channel activity. We investigated the effect of ginsenosides on human recombinant GABAA receptor (a1b1g2S) channel activity expressed in Xenopus oocytes using a two-electrode voltageclamp technique. Among the eight individual ginsenosides examined, namely, Rb1, Rb2, Rc, Rd, Re, Rf, Rg1 and Rg2, we found that Rc most potently enhanced the GABA-induced inward peak current ( IGABA). Ginsenoside Rc alone induced an inward membrane current in certain batches of oocytes expressing the GABAA receptor. The effect of ginsenoside Rc on IGABA was both dose-dependent and reversible. The half-stimulatory concentration (EC50) of ginsenoside Rc was 53.2 ± 12.3 mM. Both bicuculline, a GABAA receptor antagonist, and picrotoxin, a GABAA channel blocker, blocked the stimulatory effect of ginsenoside Rc on IGABA. Niflumic acid (NFA) and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), both Cl- channel blockers, attenuated the effect of ginsenoside Rc on IGABA. This study suggests that ginsenosides regulated GABAA receptor expressed in Xenopus oocytes and implies that this regulation might be one of the pharmacological actions of Panax ginseng.
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신태준,나승열,Hyeon-Joong Kim,Byeong-Jae Kwon,최선혜,Hyun-Bum Kim,황성희,이병환,Sang-MokLee,R. Suzanne Zukin,박지호,Hyoung Chun KIM,Hyewhon Rhim,Joon-Hee Lee 한국분자세포생물학회 2012 Molecules and cells Vol.34 No.6
Ginseng has been shown to have memory-improving effects in human. However, little is known about the active components and the molecular mechanisms underlying its effects. Recently, we isolated novel lysophosphatidic acids (LPAs)-ginseng protein complex derived from ginseng, gintonin. Gintonin activates G protein-coupled LPA receptors with high affinity. Gintonin activated Ca2+-activated Cl- channels in Xenopus oocytes through the activation of endogenous LPA receptor. In the present study, we investigated whether the activation of LPA receptor by gintonin is coupled to the regulation of N-methyl-D-aspartic acid (NMDA) receptor channel activity in Xenopus oocytes expressing rat NMDA receptors. The NMDA receptor-media-ted ion current (INMDA) was measured using the two-elec-trode voltage-clamp technique. In oocytes injected with cRNAs encoding NMDA receptor subunits, gintonin enhanced INMDA in a concentration-dependent manner. Gintonin-mediated INMDA enhancement was blocked by Ki16425, an LPA1/3 receptor antagonist. Gintonin action was blocked by a PLC inhibitor, IP3 receptor antagonist, Ca2+ chelator, and a tyrosine kinase inhibitor. The site-directed mutation of Ser1308 of the NMDA receptor, which is phosphorylated by protein kinase C (PKC), to an Ala residue, or co-expression of receptor protein tyrosine phosphatase with the NMDA receptor attenuated gintonin action. Moreover, gintonin treatment elicited a transient elevation of [Ca2+]i in cultured hippocampal neurons and elevated long-term potentiation (LTP) in both concentration-dependent manners in rat hippocampal slices. Gintonin-mediated LTP induction was abolished by Ki16425. These results indicate that gintonin-mediated INMDA potentiation and LTP induction in the hippocampus via the activation of LPA receptor might be responsible for ginseng-mediated improvement of memory-related brain functions.
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