染料木黄酮抑制血管内皮生长因子诱导的血管内皮细胞活化及蛋白激酶K活性  

Genistein inhibited the activation of vascular endothelial cell and activity of its PTK induced by vascular endothelial growth factor

作　　者：韩彬[1,2] 程道梅[2] 余小平[2] 彭晓莉[2] 贾皓[2] 

机构地区：[1]遵义医学院公共卫生学院,贵州遵义563003 [2]成都医学院公共卫生系,四川成都610083

出　　处：《成都医学院学报》2011年第3期192-195,共4页Journal of Chengdu Medical College

基　　金：国家自然科学基金(No:30972462);四川省科技厅青年基金(No:09ZQ026-036);成都医学院重点项目(No:CYZ07-001)

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。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.

关 键 词：染料木黄酮 血管内皮生长因子 蛋白激酶K 人脐静脉内皮细胞 

分 类 号：R651.2[医药卫生—外科学]