Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 오세관 | * |
dc.date.accessioned | 2016-08-28T11:08:15Z | - |
dc.date.available | 2016-08-28T11:08:15Z | - |
dc.date.issued | 2003 | * |
dc.identifier.issn | 1016-8478 | * |
dc.identifier.other | OAK-1374 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/219167 | - |
dc.description.abstract | Treatment of ginsenosides, major active ingredients of Panax ginseng, produces a variety of pharmacological or physiological responses with effects on the central and peripheral nervous systems. Recent reports showed that ginsenoside Rg2 inhibits nicotinic acetylcholine receptor-mediated Na+ influx and channel activity. In the present study, we investigated the effect of ginsenoside Rg2 on human 5-hydroxytryptamine3A (5-HT3A) receptor channel activity, which is also one of the ligand-gated ion channel families. The 5-HT 3A receptor was expressed in Xenopus oocytes, and the current was measured using the two-electrode voltage clamp technique. The ginsenoside Rg2 itself had no effect on the oocytes that were injected with H2O as well as on the oocytes that were injected with the 5-HT 3A receptor cRNA. In the oocytes that were injected with the 5-HT3A receptor cRNA, the pretreatment of ginsenoside Rg2 inhibited the 5-HT-induced inward peak current (I5-HT). The inhibitory effect of ginsenoside Rg2 on I5-HT was dose dependent and reversible. The half-inhibitory concentrations (IC50) of ginsenoside Rg2 was 22.3 ± 4.6 μM. The inhibition of I5-HT by ginsenoside Rg2 was non-competitive and voltage-independent. These results indicate that ginsenoside Rg2 might regulate the 5-HT3A receptors that are expressed in Xenopus oocytes. Further, this regulation on the ligand-gated ion channel activity by ginsenosides might be one of the pharmacological actions on Panax ginseng. ©KSMCB 2003. | * |
dc.language | English | * |
dc.title | Effects of ginsenoside Rg2 on the 5-HT3A receptor-mediated ion current in Xenopus oocytes | * |
dc.type | Article | * |
dc.relation.issue | 1 | * |
dc.relation.volume | 15 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.index | KCI | * |
dc.relation.startpage | 108 | * |
dc.relation.lastpage | 113 | * |
dc.relation.journaltitle | Molecules and Cells | * |
dc.identifier.wosid | WOS:000181333400016 | * |
dc.identifier.scopusid | 2-s2.0-0038178117 | * |
dc.author.google | Choi S. | * |
dc.author.google | Lee J.-H. | * |
dc.author.google | Oh S. | * |
dc.author.google | Rhim H. | * |
dc.author.google | Lee S.-M. | * |
dc.author.google | Nah S.-Y. | * |
dc.contributor.scopusid | 오세관(7404103757) | * |
dc.date.modifydate | 20240118133340 | * |