中文摘要：

目的探讨染料木黄酮（genistein,Gen）抗肿瘤血管生成的分子机制。方法实验以人脐静脉内皮细胞（human umbilical vein endothelial cells,HUVECs）为研究对象,通过锥虫蓝不相容试验测定Gen对HUVECs的细胞毒性,然后利用Caspase-3活性分析试剂盒测定Caspase-3活性,膜联蛋白V-异硫氰酸荧光素凋亡试剂盒测定凋亡率,蛋白激酶K（PTK）活性分析试剂盒测定PTK活性。结果 HUVECs经血管内皮生长因子（VEGF）刺激后,PTK活性升高,Gen可通过抑制PTK激酶活性,诱导VEGF处理的内皮细胞凋亡。结论 Gen可通过抑制PTK活性阻断VEGF诱导的内皮细胞活化,从而发挥抗肿瘤血管生成作用。

英文摘要：

Objective To investigate the molecular mechanism of genistein on anti tumor angiogenesis.Methods Cultured human umbilical vein endothelial cells（HUVECs） were choose as material.Apoptosis was quantified by using Annexin V-FITC apoptosis and caspase-3 activity assay kits.The cytotoxicity and death of HUVECs were quantified by trypan blue exclusion testing.Results Stimulation of human primary HUVECs by vascular endothelial grauth factor（VEGF） increased endothelial cell protein tyrosine kinase（PTK） activity.But treatment of ECs with genistein induced VEGF-loaded endothelial apoptosis.Conclusion Genistein interrupt the VEGF-sitmulated endothelial cell activation through inhibiting the PTK activity to play anti-angiogenesis role.