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dc.contributor.authorKim, Sunoh-
dc.contributor.authorNah, Seung-Yeol-
dc.contributor.authorRhim, Hyewhon-
dc.date.accessioned2024-01-21T00:01:37Z-
dc.date.available2024-01-21T00:01:37Z-
dc.date.created2021-08-31-
dc.date.issued2008-01-18-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/133817-
dc.description.abstractIn the present study, we have examined any possible involvement of L-type Ca2+ channels in ginseng-mediated neuroprotective actions. Exposure to a 50 mM KCl (high-K) produced neuronal cell death, which was blocked by a selective L-type Ca2+ channel blocker in cultured cortical neurons. When cultured cells were co-treated with ginseng total saponin (GTS) and high-K, GTS reduced high-K-induced neuronal death. Using Ca2+ imaging techniques, we found that GTS inhibited high-K-mediated acute and long-term [Ca2+](i) changes. These GTS-mediated [Ca2+](i) changes were diminished by nifedipine. Furthermore, GTS-mediated effects were also diminished by a saturating concentration of Bay K (10 mu M). After confirming the protective effect of GTS using a TUNEL assay, we found that ginsenosides Rf and Rg(3) are active components in ginseng-mediated neuroprotection. These results suggest that inhibition of L-type Ca2+ channels by ginseng could be one of the mechanisms for ginseng-mediated neuroprotection in cultured rat cortical neurons. (c) 2007 Published by Elsevier Inc.-
dc.languageEnglish-
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE-
dc.subjectCULTURED HIPPOCAMPAL-NEURONS-
dc.subjectCALCIUM CHANNELS-
dc.subjectRG(3)-
dc.subjectGINSENOSIDES-
dc.subjectCURRENTS-
dc.subjectDIHYDROPYRIDINES-
dc.subjectEXCITOTOXICITY-
dc.subjectBLOCKADE-
dc.subjectPROTEIN-
dc.titleNeuroprotective effects of ginseng saponins against L-type Ca2+ channel-mediated cell death in rat cortical neurons-
dc.typeArticle-
dc.identifier.doi10.1016/j.bbrc.2007.10.048-
dc.description.journalClass1-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.365, no.3, pp.399 - 405-
dc.citation.titleBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.citation.volume365-
dc.citation.number3-
dc.citation.startPage399-
dc.citation.endPage405-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000251663100001-
dc.identifier.scopusid2-s2.0-36549028238-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiophysics-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaBiophysics-
dc.type.docTypeArticle-
dc.subject.keywordPlusCULTURED HIPPOCAMPAL-NEURONS-
dc.subject.keywordPlusCALCIUM CHANNELS-
dc.subject.keywordPlusRG(3)-
dc.subject.keywordPlusGINSENOSIDES-
dc.subject.keywordPlusCURRENTS-
dc.subject.keywordPlusDIHYDROPYRIDINES-
dc.subject.keywordPlusEXCITOTOXICITY-
dc.subject.keywordPlusBLOCKADE-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordAuthorginsenosides-
dc.subject.keywordAuthorL-type Ca2+ channel-
dc.subject.keywordAuthorintracellular Ca2+-
dc.subject.keywordAuthorBay K-
dc.subject.keywordAuthorneuronal cell death-
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KIST Article > 2008
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