A ginsenoside-Rh1, a component of ginseng saponin, activates estrogen receptor in human breast carcinoma MCF-7 cells

J Steroid Biochem Mol Biol. 2003 Mar;84(4):463-8. doi: 10.1016/s0960-0760(03)00067-0.


We have examined the possibility that a component of Panax ginseng, ginsenoside-Rh1, acts by binding to steroid hormone receptors such as receptors for estrogen, glucocorticoid, androgen, and retinoic acid. Ginsenoside-Rh1 activated the transcription of the estrogen-responsive luciferase reporter gene in MCF-7 breast cancer cells at a concentration of 50 microM. Activation was inhibited by the specific estrogen receptor antagonist ICI 182,780, indicating that the estrogenic effect of ginsenoside-Rh1 is estrogen receptor dependent. Ginsenoside-Rh1 induction of luciferase activity was dose-dependent in CV-1 cells transiently transfected with estrogen receptor and reporter plasmids. Next, we evaluated the ability of ginsenoside-Rh1 to induce the estrogen-responsive genes in MCF-7 cells. Ginsenoside-Rh1 increased c-fos and pS2 at the mRNA levels at 24h after treatment, although the effects were not as prominent as 17beta-estradiol. Western blot analysis showed that progesterone receptor protein was induced at 24h of treatment of ginsenoside-Rh1. However, ginsenoside-Rh1 failed to activate the glucocorticoid receptor, the androgen receptor, or the retinoic acid receptor in CV-1 cells transiently transfected with the corresponding steroid hormone receptors and hormone responsive reporter plasmids. These data support our hypothesis that ginsenoside-Rh1 acts as a weak phytoestrogen, presumably by binding and activating the estrogen receptor.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Breast Neoplasms / drug therapy*
  • Dose-Response Relationship, Drug
  • Estradiol / pharmacology
  • Genes, Reporter
  • Ginsenosides / pharmacology*
  • Humans
  • Luciferases / metabolism
  • Membrane Proteins / metabolism
  • Models, Chemical
  • Plasmids / metabolism
  • Presenilin-2
  • Proto-Oncogene Proteins c-fos / metabolism
  • Receptors, Androgen / metabolism
  • Receptors, Estrogen / metabolism*
  • Receptors, Retinoic Acid / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction / drug effects
  • Time Factors
  • Transfection
  • Tumor Cells, Cultured


  • Ginsenosides
  • Membrane Proteins
  • PSEN2 protein, human
  • Presenilin-2
  • Proto-Oncogene Proteins c-fos
  • Receptors, Androgen
  • Receptors, Estrogen
  • Receptors, Retinoic Acid
  • Estradiol
  • ginsenoside Rh1
  • Luciferases