高级检索
易海维, 李彦荣, 孟依, 衣卫杰, 刘烈刚, 孙秀发, 应晨江. 红茶多酚对主动脉内皮细胞增殖抑制作用[J]. 中国公共卫生, 2007, 23(10): 1187-1188. DOI: 10.11847/zgggws2007-23-10-19
引用本文: 易海维, 李彦荣, 孟依, 衣卫杰, 刘烈刚, 孙秀发, 应晨江. 红茶多酚对主动脉内皮细胞增殖抑制作用[J]. 中国公共卫生, 2007, 23(10): 1187-1188. DOI: 10.11847/zgggws2007-23-10-19
YI Hai-wei, LI Yan-rong, MENG Yi, . Inhibiting effect of black tea polyphenols on proliferation of endothelial cell of artery[J]. Chinese Journal of Public Health, 2007, 23(10): 1187-1188. DOI: 10.11847/zgggws2007-23-10-19
Citation: YI Hai-wei, LI Yan-rong, MENG Yi, . Inhibiting effect of black tea polyphenols on proliferation of endothelial cell of artery[J]. Chinese Journal of Public Health, 2007, 23(10): 1187-1188. DOI: 10.11847/zgggws2007-23-10-19

红茶多酚对主动脉内皮细胞增殖抑制作用

Inhibiting effect of black tea polyphenols on proliferation of endothelial cell of artery

  • 摘要: 目的 观察红茶多酚对牛主动脉内皮细胞(BAECs)增殖的影响,并探讨其作用机制。方法 用四甲基偶氮噻唑蓝(MTT)检测细胞增殖活性,用蛋白免疫印迹测定p38丝裂原活化蛋白激酶(MAPK)磷酸化表达。结果 不同浓度红茶多酚对牛主动脉内皮细胞(BAECs)均有明显抑制作用,呈剂量时间依赖关系;红茶多酚(0.4mg/L)可以降低佛波酯(PMA)或血管紧张素Ⅱ(AngⅡ)刺激的细胞增殖(P<0.05),这种作用可以用还原型辅酶ⅡNADPH)氧化酶抑制剂apocynin或p38MAPK阻断剂SB203580预培养来实现;红茶多酚可以推迟血管紧张素Ⅱ刺激的p38MAPK磷酸化。结论 红茶多酚具有抑制内皮细胞增殖的作用,抑制PKC-NADPH氧化酶-p38MAPK信号途径可能是其重要机制之一。

     

    Abstract: Objective To observe the effects of black tea polyphenols on endothelial proliferation and search for the mechanism of black tea polyphenols on inhibiting cell proliferation.Methods Endothelial cell proliferation was determined by MTT assay.P38MAPK phosphorylation was measured by Western blot.Results Black tea polyphenols inhibited cell proliferations in a dose-and time-dependent manner and block endothelial cell proliferation induced by PMA or AngⅡ(<0.05).Similar blocking effect can be achieved with NADPH oxidase inhibitor,apocynin or p38MAPK pathway inhibitor SB203580.Phosphorylation analysis showed black tea polyphenols postponed the transduction of p38MAPK phosphorylation induced by AngⅡ.Conclusion Black tea polyphenols inhibited endothelial proliferation mainly via restraining or postponing the PKC-NADPH oxidase-p38MAP Kpathway.

     

/

返回文章
返回