【摘要】 目的探讨绿茶的主要成分麦没食子儿茶素没食子酸酯(EGCG)在血管内皮细胞中对肿瘤坏死因子-α(TNF-α)所诱导的纤溶酶原激活物抑制物-1(PAI-1)表达的影响及机制。方法利用人脐静脉内皮细胞体外培养方法,分别与TNF-α和/或EGCG孵育,运用蛋白免疫印迹方法检测内皮细胞中磷酸化细胞外调节蛋白激酶1/2(p-ERK1/2)和肿瘤坏死因子受体1(TNFR1)蛋白表达,应用酶联免疫吸附法方法检测细胞液中PAI-1水平。结果 TNF-α以浓度依赖和时间依赖方式增加内皮细胞中PAI-1的表达。EGCG可抑制TNF-α所诱导的PAI-1的表达,并可抑制ERK1/2磷酸化。TNF-α的刺激可使TN-FR1表达明显减少,而EGCG可抑制这一作用。结论 EGCG可能通过抑制ERK1/2的磷酸化,从而抑制TNF-α所诱导的PAI-1的表达,同时可减少TNF-α对TNFR1的抑制作用,在改善肥胖、胰岛素抵抗及相关心血管疾病中起着重要作用。更多还原

【Abstract】 Objective To investigate the effects of(-)-Epigallocatechin gallate(EGCG),the major catechin derived from green tea,on vascular endothelial TNF-α-induced plasminogen activator inhibitor-1(PAI-1) production and its mechanisms.Methods Human umbilical vein endothelial cells were cultured and incubated with TNF-α and/or EGCG.The expressions of phosphor-extracellular regulated protein kinase 1/2(p-ERK1/2) and tumor necrosis factor receptor 1(TNFR1) protein were quantified by western blotting,and PAI-1 levels were measured by enzyme-linked immunosorbent assay.Results TNF-α increased PAI-1 production in both a concentration-and time-dependent manner.EGCG prevented TNF-α-mediated PAI-1 production and reduced phosphorylation of ERK1/2.TNF-α stimulation resulted in a significant decrease in TNFR1,but EGCG prevented such decrease.Conclusion EGCG inhibits TNF-α-induced PAI-1 production.Moreover,EGCG inhibits ERK1/2 phosphorylation as well as TNF-α-mediated reduction in TNFR1,which subsequently results in reduced PAI-1 production.These data provide a novel mechanism that(-)-epigallocatechin gallate can provide direct vascular benefits in inflammatory cardiovascular diseases.更多还原