Inhibitory effects of emodin on angiogenesis.
- Author:
Xin-hua WANG
1
;
Shu-ying WU
;
Yong-su ZHEN
Author Information
- Publication Type:Journal Article
- MeSH: 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; metabolism; Fibroblast Growth Factor 2; pharmacology; Neovascularization, Physiologic; drug effects; Proto-Oncogene Proteins c-bcl-2; metabolism; Vascular Endothelial Growth Factor A; pharmacology
- From: Acta Pharmaceutica Sinica 2004;39(4):254-258
- CountryChina
- Language:English
-
Abstract:
AIMTo determine the anti-angiogenic activity of emodin.
METHODSChick embryo assay and cultured endothelial cells were used.
RESULTSEmodin 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.
CONCLUSIONEmodin shows anti-angiogenic activity and might be useful for the development of novel anti-cancer therapy.
