Non-genomic effects of ginsenoside-Re in endothelial cells via glucocorticoid receptor

FEBS Lett. 2007 May 29;581(13):2423-8. doi: 10.1016/j.febslet.2007.04.055. Epub 2007 Apr 30.


We demonstrated that ginsenoside-Re (Re), a pharmacological active component of ginseng, is a functional ligand of glucocorticoid receptor (GR) using competitive ligand-binding assay (IC(50)=156.6 nM; K(d)=49.7 nM) and reporter gene assay. Treatment with Re (1 microM) raises intracellular Ca(2+) ([Ca(2+)](i)) and nitric oxide (NO) levels in human umbilical vein endothelial cells as measured using fura-2 and 4-amino-5-methylamino-2',7'-difluorofluorescein diacetate, respectively. Western blot analysis shows that Re increased phosphorylation of endothelial nitric oxide synthase. These effects were abolished by GR antagonist RU486, siRNA targeting GR, non-selective cation channel blocker 2-aminoethyldiphenylborate, or in the absence of extracellular Ca(2+), indicating Re is indeed an agonistic ligand for the GR and the activated GR induces rapid Ca(2+) influx and NO production in endothelial cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Calcium / metabolism
  • Cells, Cultured
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / physiology*
  • Ginsenosides / chemistry
  • Ginsenosides / pharmacology*
  • Humans
  • Models, Molecular
  • Molecular Conformation
  • Nitric Oxide / biosynthesis
  • Receptors, Glucocorticoid / drug effects
  • Receptors, Glucocorticoid / physiology*
  • Umbilical Veins


  • Ginsenosides
  • Receptors, Glucocorticoid
  • Nitric Oxide
  • ginsenoside Re
  • ginsenoside Rg1
  • Calcium