NADH抗紫外线诱导的肝细胞株L02凋亡

目的 研究还原型尼克酰胺腺嘌呤二核苷酸（NADH）抗紫外线照射所致的细胞损伤的分子机制。方法 采用UVB紫外线照射正常肝细胞株L02（照射剂量为200J／m^2），实验组加／对照组不加NADH（400μg/ml）培养24h。AnnexinV/PI法检测细胞凋亡率，DNA凝胶电泳观察DNA断裂片断，流式细胞仪检测p53、Bcl-2、Bax蛋白表达。结果 NADH可明显抑制紫外线诱导的肝细胞凋亡，并且能够上调Bcl-2蛋白表达，下调p53、Bax蛋白表达。经紫外线照射后的肝细胞存在自身修复。结论 NADH能够抗紫外线诱导的细胞凋凋亡，其机制可能与上调Bcl-2，下调p53、Bax表达有关。

Effect of NADH against liver cell line L02 apoptosis induced by UVB irradiation.]

OBJECTIVE: To study the molecular mechanism behind the effect of reduced nicotinamide adenine dinucleotide (NADH) against apoptosis of liver cell line L02 induced by ultraviolet B (UVB) exposure. METHODS: L02 liver cells were exposed to UVB irradiation (200 J/m(2)) followed by a 24-hour culture in the presence or absence of NADH (400 microgram/ml). The degraded fragments of DNA in the cells were observed by agarose electrophoresis, the cell apoptosis rate determined by Annexin/V PI staining and p53, Bax and Bcl-2 proteins expression detected by flow cytometry. RESULT: NADH not only inhibited the apoptosis induced by UVB irradiation, but also up-regulated the expression of Bcl-2 protein and down-regulated expressions of p53 and Bax proteins (P<0.01). Repair of DNA strand damage was observed in L02 cells during the incubation time after irradiation. CONCLUSION: NADH significantly inhibits apoptosis induced by UVB irradiation possibly by the mechanism of up-regulating Bcl-2 expression and down-regulating p53 and Bax expressions.