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

被引：120
作者：
Leung, Kar Wah
Cheng, Yuen-Kit
Mak, Nai Ki
Chan, Kelvin K. C.
Fan, T. P. David
Wong, Ricky N. S. [1 ]
机构：
[1] Hong Kong Baptist Univ, Dept Biol, Hong Kong, Hong Kong, Peoples R China
[2] Hong Kong Baptist Univ, Dept Chem, Hong Kong, Hong Kong, Peoples R China
[3] Hong Kong Baptist Univ, Sch Chinese Med, Div Res & Dev, Hong Kong, Hong Kong, Peoples R China
[4] Univ Cambridge, Dept Pharmacol, Angiogenesis & TCM Lab, Cambridge CB2 1TN, England
来源：
FEBS LETTERS | 2006年 / 580卷 / 13期
关键词：
ginsenoside-Rg1; glucocorticoid receptor; nitric oxide; endothelial cells;
D O I：
10.1016/j.febslet.2006.04.080
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码：3211 / 3216
页数：6
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