Inhibitory effects of emodin on angiogenesis

Yao Xue Xue Bao. 2004 Apr;39(4):254-8.

Abstract

Aim: To determine the anti-angiogenic activity of emodin.

Methods: Chick embryo assay and cultured endothelial cells were used.

Results: Emodin at doses of 150 and 300 microg/egg caused 37.6% and 63.2% inhibition of angiogenesis, respectively. Emodin was shown to inhibit the proliferation of primary cultured bovine aortic endothelial cells in the absence or presence of basic-fibroblast growth factor (bFGF) or the presence of vascular endothelial growth factor (VEGF) in a dose-dependent manner. The IC50 values by MTT assay were 5.56, 8.40 or 6.91 mg x L(-1), respectively. Emodin at concentrations from 5.4 to 21.6 mg x L(-1) induced apoptosis of endothelial cells for 37.6% to 72.6%. Emodin caused endothelial cell cycle arrest at G2/M phase. After emodin treatment, there was a down-regulation of Cyclin B1, P34cdc2, and Bcl-2 protein expression while the Bax protein expression was unaffected.

Conclusion: Emodin shows anti-angiogenic activity and might be useful for the development of novel anti-cancer therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aorta / cytology
  • Apoptosis / drug effects*
  • CDC2 Protein Kinase / metabolism
  • Cattle
  • Cell Cycle / drug effects
  • Cell Division / drug effects
  • Cells, Cultured
  • Chick Embryo
  • Cyclin B / metabolism
  • Cyclin B1
  • Emodin / pharmacology*
  • Endothelial Cells / cytology*
  • Endothelial Cells / metabolism
  • Fibroblast Growth Factor 2 / pharmacology
  • Neovascularization, Physiologic / drug effects*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Vascular Endothelial Growth Factor A / pharmacology

Substances

  • Cyclin B
  • Cyclin B1
  • Proto-Oncogene Proteins c-bcl-2
  • Vascular Endothelial Growth Factor A
  • Fibroblast Growth Factor 2
  • CDC2 Protein Kinase
  • Emodin