中文摘要：

目的探讨染料木黄酮（genistein,Gen）抑制血管内皮细胞的分子机制。方法人脐静脉内皮细胞（human umbilical vein endothelial cells,HUVECs）经血管内皮生长因子（VEGF）预处理后,给予1、10、100μmol/Gen,利用酶链免疫吸附测定（ELISA）法检测基质金属蛋白酶-2/-9（matrix metalloproteinase-2/-9,MMP-2/9）及其抑制剂基质金属蛋白酶抑制因子（TIMP-）2/9的表达,蛋白免疫印迹法检测丝裂原活化蛋白激酶（MAPK）表达,胶原蛋白酶分析试剂盒检测溶胶原和明胶分解活性。结果 VEGF能促进HUVECs MMP-2/9的分泌和活性,上调氨基端激酶（JNK）和p38表达。Gen能降低MMP-2/9的分泌和活性,下调JNK和p38表达。结论 Gen可通过抑制MAPK活性,减少MMPs的生成,从而阻断VEGF诱导的内皮细胞活化。

英文摘要：

Objective To investigate the molecular mechanism underlying the activation inhibition of vascular endothelial cell induced by genistein.Methods The human umbilical vein endothelial cells（HUVECs） were treated with genistein of 1,10,100 μmol/L after treated with vascular endothelial grouth factor（VEGF）,then the expression of（MMP-2/-9 and TIMP-2/-9 were analyzed by ELISA method,MAPK expression（JNK,p38,ERK1/2） was detected with Western blot,and the collagenolytic and gelatinolytic activity were measured with collagenase assay kit and type IV collagenase assay kit.Results Stimulation of HUVECs by VEGF augmented matrix metalloproteinase-2/-9（MMP-2/-9） secretions and increased MMP-2/-9 activities,up-regulated the JNK and p38 expression.Treatment of ECs with genistein decreased production and inhibited activity of matrix metalloproteinases（MMP-2/-9）,and down-regulated the JNK and p38 expression.Conclusions Genistein interrupt the VEGF-sitmulated endothelial cell activation through inactivating MAPK,and decreasing the production of MMPs.