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Article: Protopanaxadiol and protopanaxatriol bind to glucocorticoid and oestrogen receptors in endothelial cells

TitleProtopanaxadiol and protopanaxatriol bind to glucocorticoid and oestrogen receptors in endothelial cells
Authors
KeywordsAngiogenesis
Endothelial cell
Ginsenoside
Intracellular calcium concentration
Nitric oxide
Nuclear receptor
Issue Date2009
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2009, v. 156 n. 4, p. 626-637 How to Cite?
AbstractBackground and purpose: Ginsenosides are used widely for medicinal purposes, but the mechanisms of their action are still unclear, although there is some evidence that these effects are mediated by nuclear receptors. Here we examined whether two metabolites of ginsenoside, protopanaxadiol (g-PPD) and protopanaxatriol (g-PPT), could modulate endothelial cell functions through the glucocorticoid receptor (GR) and oestrogen receptor (ER). Experiment approaches: The effects of g-PPD and g-PPT on intracellular calcium ion concentration ([Ca 2+] i) and nitric oxide (NO) production in human umbilical vein endothelial cells (HUVECs) were measured using Fura-2-acetoxymethyl ester, 4-amino-5-methylamino-2′,7′- difluorofluorescein and Griess reagent. Effects on expression of GR and ER isoforms in HUVECs were determined using reverse transcriptase-/real-time PCR and immunocytochemistry. Phosphorylation of endothelial NO synthase (eNOS) was assessed by Western blotting. Results: Ginsenoside protopanaxadiol and g-PPT increased [Ca 2+] i, eNOS phosphorylation and NO production in HUVECs, which were inhibited by the GR antagonist, RU486, the ER antagonist, ICI 182,780 and siRNA targeting GR or ERβ. The NO production was Ca 2+-dependent and the [Ca 2+] i elevation in HUVECs resulted from both intracellular Ca 2+ release and extracellular Ca 2+ influx. Conclusions and implications: Ginsenoside protopanaxadiol and g-PPT were functional ligands for both GR and ERβ, through which these ginsenoside metabolites exerted rapid, non-genomic effects on endothelial cells. © 2009 The British Pharmacological Society.
Persistent Identifierhttp://hdl.handle.net/10722/169856
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, KWen_HK
dc.contributor.authorLeung, FPen_HK
dc.contributor.authorMak, NKen_HK
dc.contributor.authorTombranTink, Jen_HK
dc.contributor.authorHuang, Yen_HK
dc.contributor.authorWong, RNen_HK
dc.date.accessioned2012-10-25T04:57:06Z-
dc.date.available2012-10-25T04:57:06Z-
dc.date.issued2009en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2009, v. 156 n. 4, p. 626-637en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/169856-
dc.description.abstractBackground and purpose: Ginsenosides are used widely for medicinal purposes, but the mechanisms of their action are still unclear, although there is some evidence that these effects are mediated by nuclear receptors. Here we examined whether two metabolites of ginsenoside, protopanaxadiol (g-PPD) and protopanaxatriol (g-PPT), could modulate endothelial cell functions through the glucocorticoid receptor (GR) and oestrogen receptor (ER). Experiment approaches: The effects of g-PPD and g-PPT on intracellular calcium ion concentration ([Ca 2+] i) and nitric oxide (NO) production in human umbilical vein endothelial cells (HUVECs) were measured using Fura-2-acetoxymethyl ester, 4-amino-5-methylamino-2′,7′- difluorofluorescein and Griess reagent. Effects on expression of GR and ER isoforms in HUVECs were determined using reverse transcriptase-/real-time PCR and immunocytochemistry. Phosphorylation of endothelial NO synthase (eNOS) was assessed by Western blotting. Results: Ginsenoside protopanaxadiol and g-PPT increased [Ca 2+] i, eNOS phosphorylation and NO production in HUVECs, which were inhibited by the GR antagonist, RU486, the ER antagonist, ICI 182,780 and siRNA targeting GR or ERβ. The NO production was Ca 2+-dependent and the [Ca 2+] i elevation in HUVECs resulted from both intracellular Ca 2+ release and extracellular Ca 2+ influx. Conclusions and implications: Ginsenoside protopanaxadiol and g-PPT were functional ligands for both GR and ERβ, through which these ginsenoside metabolites exerted rapid, non-genomic effects on endothelial cells. © 2009 The British Pharmacological Society.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_HK
dc.relation.ispartofBritish Journal of Pharmacologyen_HK
dc.subjectAngiogenesisen_HK
dc.subjectEndothelial cellen_HK
dc.subjectGinsenosideen_HK
dc.subjectIntracellular calcium concentrationen_HK
dc.subjectNitric oxideen_HK
dc.subjectNuclear receptoren_HK
dc.titleProtopanaxadiol and protopanaxatriol bind to glucocorticoid and oestrogen receptors 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.doi10.1111/j.1476-5381.2008.00066.xen_HK
dc.identifier.pmid19226254-
dc.identifier.scopuseid_2-s2.0-65349185491en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65349185491&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume156en_HK
dc.identifier.issue4en_HK
dc.identifier.spage626en_HK
dc.identifier.epage637en_HK
dc.identifier.isiWOS:000263450000007-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLeung, KW=13106059300en_HK
dc.identifier.scopusauthoridLeung, FP=8615375300en_HK
dc.identifier.scopusauthoridMak, NK=35587830100en_HK
dc.identifier.scopusauthoridTombranTink, J=7003724753en_HK
dc.identifier.scopusauthoridHuang, Y=7501573013en_HK
dc.identifier.scopusauthoridWong, RN=35088944900en_HK

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