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为研究细胞辅酶NADH在细胞辐射凋亡损伤中的防护作用 ,将L0 2肝细胞经 5 0Gy照射后加入不同浓度 (0～ 6 0 0 μg/ml)的NADH ,培养 6、12、2 4h ,观察细胞凋亡率并检测 3组Fas,Bax ,Bcl 2蛋白表达 ,透射电镜观察细胞凋亡形态。结果表明 ,辐射可以诱导细胞凋亡损伤 ,NADH抑制细胞辐射诱导的凋亡呈剂量依赖性 ,并可以上调Bcl 2蛋白和下调Fas、Bax蛋白表达。提示NADH对L0 2肝细胞有明显的抗辐射凋亡损伤作用 ,其作用机制可能与Fas、Bcl 2和Bax的调控有关
In order to study the protective effect of cellular coenzyme NADH on apoptosis of cell radiation, L0 2 hepatocytes were irradiated with 50 Gy of different concentrations (0 ~ 600 μg / ml) of NADH and cultured for 6, 12, 24 h, The apoptosis rate was observed and the expressions of Fas, Bax and Bcl2 protein were detected in three groups. The morphological changes of apoptosis were observed by transmission electron microscope. The results showed that radiation could induce cell apoptosis injury, NADH inhibited cell radiation-induced apoptosis in a dose-dependent manner, and up-regulated Bcl 2 protein and down-regulated Fas and Bax protein expression. These results suggest that NADH has a significant anti-apoptotic effect on L0 2 hepatocytes and its mechanism may be related to the regulation of Fas, Bcl 2 and Bax