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Article: Signaling pathway of ginsenoside-Rg1 leading to nitric oxide production in endothelial cells

TitleSignaling pathway of ginsenoside-Rg1 leading to nitric oxide production in endothelial cells
Authors
KeywordsEndothelial cells
Ginsenoside-Rg1
Glucocorticoid receptor
Nitric oxide
Issue Date2006
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/febslet
Citation
Febs Letters, 2006, v. 580 n. 13, p. 3211-3216 How to Cite?
AbstractWe here provide definitive evidence that ginsenoside-Rg1, the pharmacologically active component of ginseng, is a functional ligand of the glucocorticoid receptor (GR) as determined by fluorescence polarization assay. Rg1 increased the phosphorylation of GR, phosphatidylinositol-3 kinase (PI3K), Akt/PKB and endothelial nitric oxide synthase (eNOS) leading to increase nitric oxide (NO) production in human umbilical vein endothelial cell. Rg1-induced eNOS phosphorylation and NO production were significantly reduced by RU486, LY294,002, or SH-6. Also, knockdown of GR completely eliminated the Rg1-induced NO production. This study revealed that Rg1 can indeed serve as an agonist ligand for GR and the activated GR can induce rapid NO production from eNOS via the non-transcriptional PI3K/Akt pathway. © 2006 Federation of European Biochemical Societies.
Persistent Identifierhttp://hdl.handle.net/10722/169847
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.authorCheng, YKen_HK
dc.contributor.authorMak, NKen_HK
dc.contributor.authorChan, KKCen_HK
dc.contributor.authorDavid Fan, TPen_HK
dc.contributor.authorWong, RNSen_HK
dc.date.accessioned2012-10-25T04:57:02Z-
dc.date.available2012-10-25T04:57:02Z-
dc.date.issued2006en_HK
dc.identifier.citationFebs Letters, 2006, v. 580 n. 13, p. 3211-3216en_HK
dc.identifier.issn0014-5793en_HK
dc.identifier.urihttp://hdl.handle.net/10722/169847-
dc.description.abstractWe here provide definitive evidence that ginsenoside-Rg1, the pharmacologically active component of ginseng, is a functional ligand of the glucocorticoid receptor (GR) as determined by fluorescence polarization assay. Rg1 increased the phosphorylation of GR, phosphatidylinositol-3 kinase (PI3K), Akt/PKB and endothelial nitric oxide synthase (eNOS) leading to increase nitric oxide (NO) production in human umbilical vein endothelial cell. Rg1-induced eNOS phosphorylation and NO production were significantly reduced by RU486, LY294,002, or SH-6. Also, knockdown of GR completely eliminated the Rg1-induced NO production. This study revealed that Rg1 can indeed serve as an agonist ligand for GR and the activated GR can induce rapid NO production from eNOS via the non-transcriptional PI3K/Akt pathway. © 2006 Federation of European Biochemical Societies.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.subjectEndothelial cellsen_HK
dc.subjectGinsenoside-Rg1en_HK
dc.subjectGlucocorticoid receptoren_HK
dc.subjectNitric oxideen_HK
dc.subject.meshChromones - Pharmacologyen_US
dc.subject.meshEndothelial Cells - Drug Effects - Metabolismen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshGinsenosides - Metabolism - Pharmacologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMifepristone - Pharmacologyen_US
dc.subject.meshMorpholines - Pharmacologyen_US
dc.subject.meshNitric Oxide - Biosynthesisen_US
dc.subject.meshNitric Oxide Synthase Type Iii - Drug Effects - Metabolismen_US
dc.subject.meshPhosphatidylinositol 3-Kinases - Metabolismen_US
dc.subject.meshPhosphorylationen_US
dc.subject.meshProtein Transport - Drug Effectsen_US
dc.subject.meshProto-Oncogene Proteins C-Akt - Metabolismen_US
dc.subject.meshReceptors, Glucocorticoid - Agonists - Genetics - Metabolismen_US
dc.subject.meshSignal Transductionen_US
dc.titleSignaling pathway of ginsenoside-Rg1 leading to nitric oxide production in endothelial cellsen_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.2006.04.080en_HK
dc.identifier.pmid16696977-
dc.identifier.scopuseid_2-s2.0-33646556664en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33646556664&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume580en_HK
dc.identifier.issue13en_HK
dc.identifier.spage3211en_HK
dc.identifier.epage3216en_HK
dc.identifier.isiWOS:000238107400034-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridLeung, KW=13106059300en_HK
dc.identifier.scopusauthoridCheng, YK=9133925600en_HK
dc.identifier.scopusauthoridMak, NK=35587830100en_HK
dc.identifier.scopusauthoridChan, KKC=25633775800en_HK
dc.identifier.scopusauthoridDavid Fan, TP=13410504200en_HK
dc.identifier.scopusauthoridWong, RNS=7402126957en_HK

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