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作 者:曹艳丽[1] 王涤非[1] 王晓黎[1] 孟馨[1] 张锦[1] 单忠艳[1]
机构地区:[1]中国医科大学附属第一医院内分泌科,中国医科大学内分泌疾病研究所,辽宁省内分泌疾病重点实验室
出 处:《中国组织化学与细胞化学杂志》2012年第5期453-456,共4页Chinese Journal of Histochemistry and Cytochemistry
基 金:国家自然科学基金青年基金(81000327);辽宁省自然科学基金(20092113);辽宁省科学技术计划(201022502);辽宁省教育厅科研项目计划(L2010626)
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。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 blot- ting, 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 de- crease 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 (-)-epigallocateehin gallate can provide direct vascular benefits in inflammatory cardiovascular disea- ses.
关 键 词:麦没食子儿茶素没食子酸酯 肿瘤坏死因子-α 肥胖 纤溶酶原激活物抑制物-1 血管疾病
分 类 号:R329-33[医药卫生—人体解剖和组织胚胎学]
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