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Article: Non-genomic effects of ginsenoside-Re in endothelial cells via glucocorticoid receptor

TitleNon-genomic effects of ginsenoside-Re in endothelial cells via glucocorticoid receptor
Authors
KeywordsAngiogenesis
Endothelial cell
Ginsenoside
Glucocorticoid receptor
Intracellular calcium concentration
Nitric oxide
Issue Date2007
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/febslet
Citation
Febs Letters, 2007, v. 581 n. 13, p. 2423-2428 How to Cite?
AbstractWe demonstrated that ginsenoside-Re (Re), a pharmacological active component of ginseng, is a functional ligand of glucocorticoid receptor (GR) using competitive ligand-binding assay (IC50 = 156.6 nM; Kd = 49.7 nM) and reporter gene assay. Treatment with Re (1 μM) raises intracellular Ca2+ ([Ca2+]i) and nitric oxide (NO) levels in human umbilical vein endothelial cells as measured using fura-2 and 4-amino-5-methylamino-2′,7′-difluorofluorescein diacetate, respectively. Western blot analysis shows that Re increased phosphorylation of endothelial nitric oxide synthase. These effects were abolished by GR antagonist RU486, siRNA targeting GR, non-selective cation channel blocker 2-aminoethyldiphenylborate, or in the absence of extracellular Ca2+, indicating Re is indeed an agonistic ligand for the GR and the activated GR induces rapid Ca2+ influx and NO production in endothelial cells. © 2007.
Persistent Identifierhttp://hdl.handle.net/10722/169850
ISSN
2015 Impact Factor: 3.519
2015 SCImago Journal Rankings: 2.026
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, KWen_HK
dc.contributor.authorLeung, FPen_HK
dc.contributor.authorHuang, Yen_HK
dc.contributor.authorMak, NKen_HK
dc.contributor.authorWong, RNSen_HK
dc.date.accessioned2012-10-25T04:57:03Z-
dc.date.available2012-10-25T04:57:03Z-
dc.date.issued2007en_HK
dc.identifier.citationFebs Letters, 2007, v. 581 n. 13, p. 2423-2428en_HK
dc.identifier.issn0014-5793en_HK
dc.identifier.urihttp://hdl.handle.net/10722/169850-
dc.description.abstractWe demonstrated that ginsenoside-Re (Re), a pharmacological active component of ginseng, is a functional ligand of glucocorticoid receptor (GR) using competitive ligand-binding assay (IC50 = 156.6 nM; Kd = 49.7 nM) and reporter gene assay. Treatment with Re (1 μM) raises intracellular Ca2+ ([Ca2+]i) and nitric oxide (NO) levels in human umbilical vein endothelial cells as measured using fura-2 and 4-amino-5-methylamino-2′,7′-difluorofluorescein diacetate, respectively. Western blot analysis shows that Re increased phosphorylation of endothelial nitric oxide synthase. These effects were abolished by GR antagonist RU486, siRNA targeting GR, non-selective cation channel blocker 2-aminoethyldiphenylborate, or in the absence of extracellular Ca2+, indicating Re is indeed an agonistic ligand for the GR and the activated GR induces rapid Ca2+ influx and NO production in endothelial cells. © 2007.en_HK
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/febsleten_HK
dc.relation.ispartofFEBS Lettersen_HK
dc.subjectAngiogenesisen_HK
dc.subjectEndothelial cellen_HK
dc.subjectGinsenosideen_HK
dc.subjectGlucocorticoid receptoren_HK
dc.subjectIntracellular calcium concentrationen_HK
dc.subjectNitric oxideen_HK
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshGinsenosides - Chemistry - Pharmacologyen_US
dc.subject.meshHumansen_US
dc.subject.meshModels, Molecularen_US
dc.subject.meshMolecular Conformationen_US
dc.subject.meshNitric Oxide - Biosynthesisen_US
dc.subject.meshReceptors, Glucocorticoid - Drug Effects - Physiologyen_US
dc.subject.meshUmbilical Veinsen_US
dc.titleNon-genomic effects of ginsenoside-Re in endothelial cells via glucocorticoid receptoren_HK
dc.typeArticleen_HK
dc.identifier.emailLeung, KW: kwleung1@hku.hken_HK
dc.identifier.authorityLeung, KW=rp01674en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.febslet.2007.04.055en_HK
dc.identifier.pmid17490654-
dc.identifier.scopuseid_2-s2.0-34248590312en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34248590312&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume581en_HK
dc.identifier.issue13en_HK
dc.identifier.spage2423en_HK
dc.identifier.epage2428en_HK
dc.identifier.isiWOS:000247087600007-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridLeung, KW=13106059300en_HK
dc.identifier.scopusauthoridLeung, FP=8615375300en_HK
dc.identifier.scopusauthoridHuang, Y=34770945300en_HK
dc.identifier.scopusauthoridMak, NK=35587830100en_HK
dc.identifier.scopusauthoridWong, RNS=7402126957en_HK

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