中文摘要：

目的：探索H2O2对TNF—α诱导血管内皮细胞凋亡的作用及异丙酚（propofol）对细胞凋亡的保护作用和可能的机制。方法：将体外培养的ECV304细胞分为5组：①对照组（Control）；②10μmol／L H2O2组（H）；③40nmol／L TNF—α组（T）；④TNF—α＋H2O2组（T＋H）；⑤TNF—α＋H2O2＋propofol组（T＋H＋P）。观察：①流式细胞仪检测细胞凋亡率；②丙二醛（MDA）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH—Px）含量。结果：10μmol／L的H2O2仅造成少量细胞凋亡，MDA含量变化不显著（P〉0．05）；与TNF-α共同作用后细胞凋亡率显著增加，且高于二者分别作用之和，细胞内MDA含量也明显增加，SOD和GSH—Px含量明显减少，与TNF-α组相比差异具有显著性（P〈0．05）；加入异丙酚预处理可使TNF-α和H2O2组凋亡率明显降低，同时伴随细胞内MDA含量降低，SOD和GSH—Px含量增加。结论：H2O2能显著增强TNF-α诱导细胞凋亡的效应，异丙酚通过降低细胞氧化损伤的机制，有效逆转H2O2增强TNF-α诱导细胞凋亡的效应。

英文摘要：

Objective： To test the hypothesis that oxygen free radicals can potentiate TNF-α cellular toxicity, which might be reserved by propofol in human vascular endothelial cells. Methods： Cultured human ECV304 cells were divided into five groups： untreated （Control）, treated with 10 μmol/L hydrogen peroxide （H2O2 ） and treated with 40 nmol/L TNF-α alone （T） or in the presence of H2O2（T＋H） or inpropofol ＋ H2O2（T＋H＋P）, with each cultured for 24 hours. Cell apoptosis was assessed by flow cytometry. The concentration of malondialdehyde （MDA）, super-oxide dismutase.（SOD） and glutathione peroxidase （GSH-Px） were detected at the same time. Results： H2O2, at 10 μmol/L, did not cause significant lipid peroxidation, but enhanced TNF-α induced cell apoptosis（P〈0.01）. Propofol at 50μmol/L attenuated TNF-α and H2O2 induced cell apoptosis, accompanied with a decrease in MDA, while with increases in SOD and GSH-Px.Conclusion. H2O2, even at trace concentration, may significantly enhance TNF-α induced endothelial cell apoptosis. Propofol exerts protective effects against H2O2 potentiated TNF-α cell toxicity by reduction of oxidative injury.