Signaling pathway of ginsenoside-Rg1 leading to nitric oxide production in endothelial cells
Signaling pathway of ginsenoside-Rg1 leading to nitric oxide production in endothelial cells
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DOI：
10.1016/j.febslet.2006.04.080
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发表时间：
2006-05-29
期刊：
影响因子：
3.5
通讯作者：
Wong, Ricky N. S.
中科院分区：
文献类型：
--
作者：
Leung, Kar Wah;Cheng, Yuen-Kit;Wong, Ricky N. S.
我们在此提供了明确的证据，证明人参的药理活性成分人参皂苷-Rg1是糖皮质激素受体(GR)的功能配体。Rg1上调人脐静脉内皮细胞GR、磷脂酰肌醇-3激酶(PI3K)、Akt/PKB和内皮型一氧化氮合酶(ENOS)的磷酸化，从而增加一氧化氮(NO)的产生。RU486、LY294,002或SH-6可显著降低Rg1诱导的eNOS磷酸化和NO生成。此外，GR基因敲除可完全消除Rg1诱导的NO生成。本研究表明，Rg1确实可以作为GR的激动剂配体，并且激活的GR可以通过非转录的PI3K/Akt途径诱导eNOS快速产生NO。(C)2006年欧洲生化学会联合会。爱思唯尔出版，版权所有。
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.