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目的 探讨金粉蕨素拮抗Menadione氧化损伤所抑制的内皮细胞增殖的作用及其机制。方法 以Menadione(O- 2 )损伤人脐静脉内皮细胞作为氧化损伤模型 ,采用MTT法和细胞计数法 ,观察不同浓度金粉蕨素对Menadione损伤内皮细胞生长抑制率的影响 ;利用硝酸还原酶法测定培养液中NO含量 ;以Westernblot检测细胞eNOS活性及磷酸化ERK1 / 2的表达。结果 金粉蕨素保护组与损伤组相比 ,内皮细胞的生长抑制率明显降低 ,培养液中NO含量增高 ,eNOS活性增强 ,磷酸化ERK1 / 2表达上调。结论 NO和ERK1 / 2通路可能介导了金粉蕨素拮抗Menadione氧化损伤所抑制内皮细胞增殖的保护作用
Objective To investigate the effect and mechanism of acantholing on the proliferation of endothelial cells inhibited by oxidative injury of Menadione. Methods The human umbilical vein endothelial cells were injured by Menadione(O-2) as an oxidative injury model. The effects of different concentrations of orononin on the proliferation inhibition rate of Menadione injured endothelial cells were observed by MTT method and cell counting method. The content of NO in the culture medium was detected by Western blot, and the expression of eNOS activity and ERK1 / 2 phosphorylation was detected. Results Compared with the injury group, the amphotericin-protected group showed a significant decrease in endothelial cell growth inhibition rate, increased NO content in culture medium, enhanced eNOS activity, and increased expression of phosphorylated ERK1 / 2. Conclusions NO and ERK1 / 2 pathway may mediate the protective effect of abelrin on oxidative injury induced by Menadione in endothelial cells.