2004PubMedRequires access

Inhibitory effects of emodin on angiogenesis.

Xin-hua Wang, Shu-ying Wu, Yong‐Su Zhen

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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.

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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.

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Available 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.

Key concepts: Emodin, Angiogenesis, Basic fibroblast growth factor, Apoptosis, MTT assay, Endothelial stem cell, Vascular endothelial growth factor, Chemistry

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