NADH对辐射诱导正常肝细胞株L02损伤时细胞凋亡的影响

Effect of NADH on apoptosis during radiation injury of liver cell line L02

目的研究抗氧化剂NADH对5.0 GyX射线照射正常细胞的防护作用.方法处理组于5.0 Gy X射线照射后立即加入NADH,一次给药,剂量为100～600 μg/ml,分别观察培养6、12、24 h后凋亡细胞率及p53和Bcl-2蛋白表达,并且与照射后加入RPMI 1640组和假照射组比较.结果NADH抑制细胞凋亡率呈剂量依赖性,在浓度为400～600 μg/ml时达平台,并且能够上调Bcl-2蛋白表达,下p53蛋白表达,差异非常显著(P＜0.01).结论NADH对受照L02肝细胞有明显的防护作用,但其作用机制还需进一步研究.

Objective To study the radiaoprotective effect of the antioxidant NADH on normal liver cell lines. Methods L02 liver cells were cultured in RPMI 1640 supplemented with 10% fetal bovine serum and exposed to 5.0 Gy X-rays, with subsequent culture in the presence or absence of different concentrations of NADH for 6, 12 and 24 h. The ratio of apoptotic cells, p53 protein and Bcl-2 protein expressions were then determined. Results NADH significantly inhibited the apoptosis of liver cell line L02 in a dose-dependant manner, and when the concentration of NADH had reached to 400 μg/ml, the apoptosis rate dropped only slightly with further concentration increase. NADH, at the same time, could upregulate the expression of Bcl-2 protein and downregulate that of p53 protein (P<0.01). Conclusion NADH has marked radioprotective effect but its mechanism needs further investigation.