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dc.contributor.authorLeung, Kar Wah
dc.contributor.authorCheng, Yuen-Kit
dc.contributor.authorMak, Nai Ki
dc.contributor.authorChan, Kelvin C.
dc.contributor.authorFan, T. P. David
dc.contributor.authorWong, Ricky N. S.
dc.date.accessioned2007-03-07T13:53:05Z
dc.date.available2007-03-07T13:53:05Z
dc.date.issued2006
dc.date.submitted2007-02-01
dc.identifier.citationFEBS Letters, 580(13): 3211-3216
dc.identifier.issn0014-5793
dc.identifier.pmid16696977
dc.identifier.doi10.1016/j.febslet.2006.04.080
dc.identifier.urihttp://hdl.handle.net/2436/9833
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.
dc.format.extent395944 bytes
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.publisherElsevier
dc.relation.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0014579306005370
dc.subjectGinsenoside-Rg1
dc.subjectNitric acid
dc.subjectEndothelial cells
dc.titleSignaling pathway of ginsenoside-Rg1 leading to nitric oxide production in endothelial cells.
dc.typeJournal article
dc.identifier.journalFEBS Letters
dc.format.digYES
refterms.dateFOA2018-08-22T07:14:56Z
html.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.


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