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

Kar Wah Leung; Yuen-Kit Cheng; Nai Ki Mak; Kelvin Chan; Tai Ping Fan; Ricky N. S. Wong

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

Kar Wah Leung, Yuen-Kit Cheng, Nai Ki Mak, Kelvin Chan, Tai Ping Fan, Ricky N. S. Wong

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Abstract

We 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.

Original language	English
Pages (from-to)	3211-3216
Number of pages	6
Journal	FEBS Letters
Volume	580
Issue number	13
Publication status	Published - 2006

Keywords

glucocorticoids
nitric oxide

Cite this

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title = "Signaling pathway of ginsenoside-Rg1 leading to nitric oxide production in endothelial cells",

abstract = "We 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.",

keywords = "glucocorticoids, nitric oxide",

author = "Leung, {Kar Wah} and Yuen-Kit Cheng and Mak, {Nai Ki} and Kelvin Chan and Fan, {Tai Ping} and Wong, {Ricky N. S.}",

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TY - JOUR

T1 - Signaling pathway of ginsenoside-Rg1 leading to nitric oxide production in endothelial cells

AU - Leung, Kar Wah

AU - Cheng, Yuen-Kit

AU - Mak, Nai Ki

AU - Chan, Kelvin

AU - Fan, Tai Ping

AU - Wong, Ricky N. S.

PY - 2006

Y1 - 2006

N2 - We 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.

AB - We 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.

KW - glucocorticoids

KW - nitric oxide

UR - http://handle.uws.edu.au:8081/1959.7/506283

M3 - Article

SN - 0014-5793

VL - 580

SP - 3211

EP - 3216

JO - FEBS Letters

JF - FEBS Letters

IS - 13

ER -

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

Abstract

Keywords

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