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目的 探讨过氧化氢 (H2 O2 )对人脐静脉内皮细胞株 (ECV 30 4)的损伤作用及其可能机制。方法 对体外培养的ECV 30 4,采用形态学、琼脂糖凝胶电泳及流式细胞术等方法 ,观察过氧化氢的损伤方式及调控基因蛋白Fas和bcl 2的影响。结果 一定剂量 ( 10 0、30 0、5 0 0mmol/L)的过氧化氢刺激后 ,内皮细胞发生凋亡 ,凋亡率分别是 8.38± 2 .19、14 .60± 2 .75、2 0 .63± 3.89,与对照组 2 .38± 0 .96相比 ,差异具有非常显著性 ( P <0 .0 1)。同时Fas蛋白显著增加 ,分别为17.0 3± 5 .5 9、2 0 .38± 7.0 2、2 7.60± 4.5 5 ,bcl 2蛋白明显下调 ,分别为 19.35± 3.36、18.75± 3.33、13.0 5± 2 .93,与对照组相比差异均具有显著性 (P <0 .0 5或P <0 .0 1)。结论 一定剂量的过氧化氢对血管内皮细胞的损伤可通过诱导Fas表达增加 ,bcl 2表达下调 ,而致细胞凋亡。
Objective To investigate the injury effect of hydrogen peroxide (H2O2) on human umbilical vein endothelial cell line (ECV 30 4) and its possible mechanism. Methods The ECV 30 4 cells cultured in vitro were stained with morphological, agarose gel electrophoresis and flow cytometry to observe the damage of hydrogen peroxide and the effects of regulating gene proteins Fas and bcl 2. Results After stimulated by hydrogen peroxide at a certain dose (10 0, 30 0, 500 mmol / L), the apoptosis of endothelial cells was observed. The apoptotic rate was 8.38 ± 2.19, 14.60 ± 2.75, 20 .63 ± 3.89, compared with the control group 2.38 ± 0.96, the difference was very significant (P <0.01). At the same time, Fas protein increased significantly (17.0 3 ± 5 .5 9,2 0 .38 ± 7.0 2, 7.60 ± 4.5 5, respectively), and the levels of bcl 2 protein were significantly decreased, which were 19.35 ± 3.36,18.75 ± 3.33,13.0 5 ± 2 .93, compared with the control group, the difference was significant (P <0.05 or P <0.01). Conclusion The hydrogen peroxide at a certain dose can damage the vascular endothelial cells by inducing the increase of Fas expression and the decrease of bcl-2 expression, leading to cell apoptosis.