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目的 研究抗氧化剂NADH对体外培养的正常人肝细胞系L0 2缺血再灌注损伤的保护作用及可能的机制。方法 实验分组 :将培养的L0 2细胞分为 :缺血再灌注损伤组 (I R) ,缺血再灌注损伤 +NADH(I R +NADH)及对照组 (未经处理的L0 2细胞 )。用流式细胞仪观察细胞处理后6、12、18及 2 4h细胞的凋亡率及 12h时 ,Bcl 2、Bax、P5 3、CD95及CD95L的表达 ,并以透射电镜观察细胞凋亡的超微结构。结果 NADH可明显抑制缺血再灌注损伤细胞的凋亡 ,并能上调Bcl 2表达 ,下调Bax、P5 3、CD95及CD95L的表达 ,与I R组相比较差异显著 (P <0 .0 5 )。透射电镜下可见典型的凋亡细胞的特征。结论 NADH对缺血再灌注损伤诱导的L0 2肝细胞有明显地保护作用。其作用机制可能与通过调节Bcl 2、Bax、P5 3、CD95及CD95L的表达有关
Objective To study the protective effect and possible mechanism of antioxidant NADH on L0 2 ischemia-reperfusion injury in normal human hepatocyte line cultured in vitro. Methods The experimental groups were divided into three groups: ischemia-reperfusion injury group (I R), ischemia-reperfusion injury + NADH (I R + NADH) and control group (untreated L0 2 cells). The apoptosis rate of cells at 6, 12, 18 and 24 h after treatment and the expression of Bcl 2, Bax, P 5 3, CD95 and CD95L at 12h were observed by flow cytometry. The apoptosis rate microstructure. Results NADH could significantly inhibit the apoptosis of ischemia-reperfusion-injury cells and up-regulate the expression of Bcl-2 and down-regulate the expressions of Bax, P53, CD95 and CD95L, which are significantly different from those of IR (P <0.05). The characteristics of typical apoptotic cells can be seen under transmission electron microscope. Conclusion NADH can obviously protect L02 hepatocytes induced by ischemia-reperfusion injury. Its mechanism may be related to the regulation of Bcl 2, Bax, P5 3, CD95 and CD95L expression