目的:探讨核因子-E2相关因子2（Nrf2）信号通路在亚砷酸钠（NaAsOn 2）致人正常肝细胞（L-02细胞）氧化损伤过程中的作用，为砷致肝损伤的氧化损伤作用机制研究提供实验依据。n 方法:体外培养L-02细胞，分别以0（对照）、25、50、75、100、125、150 μmol/L NaAsOn 2处理细胞24 h，采用CCK8法检测细胞存活率；根据细胞存活率计算半抑制浓度（ICn 50），分别以ICn 50的0、1/8、1/4、1/2倍剂量NaAsOn 2处理L-02细胞进行分组实验。采用蛋白免疫印迹法（Western blot）检测L-02细胞中和细胞核内Nrf2信号通路相关因子Nrf2、血红素氧化酶-1（HO-1）、醌氧化还原酶1（NQO1）、谷胱甘肽过氧化物酶1（GPx1）的蛋白表达情况。n 结果:CCK8实验结果显示，25、50、75、100、125、150 μmol/L NaAsOn 2组的L-02细胞存活率[（69.53 ± 0.06）%、（41.33 ± 0.08）%、（23.65 ± 0.04）%、（26.51 ± 0.04）%、（31.63 ± 0.01）%、（26.24 ± 0.02）%]明显低于对照组[（100.00 ± 0.00）%，n P均< 0.05]；细胞存活率的ICn 50为40 μmol/L，分组实验的NaAsOn 2剂量分别采用0（对照）、5、10、20 μmol/L。Western blot检测结果显示，与对照组比较，5、10、20 μmol/L NaAsOn 2组L-02细胞中Nrf2、HO-1及L-02细胞核内HO-1蛋白水平显著升高（n P均< 0.05）；10、20 μmol/L NaAsOn 2组L-02细胞中GPx1蛋白水平显著降低（n P均< 0.05），L-02细胞核内Nrf2蛋白水平显著升高（n P均< 0.05）；5 μmol/L NaAsOn 2组L-02细胞核内NQO1蛋白水平显著升高（n P < 0.05）。n 结论:NaAsOn 2对L-02细胞中Nrf2信号通路相关因子的表达有影响，其致L-02细胞氧化损伤的作用机制可能与Nrf2信号通路有关。n “,”Objective:To explore the role of nuclear factor-E2-related factor 2 (Nrf2) signaling pathway in oxidative damage caused by sodium arsenite (NaAsOn 2) in human normal liver cells (L-02), and to provide experimental basis for the study of oxidative damage mechanism of liver damage caused by arsenic.n Methods:L-02 cells were cultured n in vitro and treated with 0 (control), 25, 50, 75, 100, 125, and 150 μmol/L NaAsO n 2, respectively, for 24 h. The half-inhibitory concentration (ICn 50) was calculated according to the cell survival rate by CCK8, and L-02 cells were treated with 0, 1/8, 1/4 and 1/2 dose of ICn 50 of NaAsOn 2, respectively, for grouping experiments. Protein expressions of Nrf2, heme oxygenase-1 (HO-1), NADH quinone oxidoreductase 1 (NQO1) and glutathione peroxidase 1 (GPx1) in L-02 cells and L-02 nucleus were detected by Western blotting.n Results:The result of CCK8 showed that the survival rates of L-02 cells in 25, 50, 75, 100, 125, 150 μmol/L NaAsO n 2 groups were [(69.53 ± 0.06)%, (41.33 ± 0.08)%, (23.65 ± 0.04)%, (26.51 ± 0.04)%, (31.63 ± 0.01)%, (26.24 ± 0.02)%], which were significantly lower than that of the control group[(100 ± 0.00)%]. The differences were statistically significant (n P < 0.05). The IC n 50 calculated by cell survival was 40 μmol/L, and the NaAsO n 2 doses used in the experiment were 0 (control), 5, 10, and 20 μmol/L. Western blotting results showed that, compared with the control group, the protein expression levels of Nrf2, HO-1 in L-02 and HO-1 in the L-02 cells nucleus in the 5, 10 and 20 μmol/L NaAsO n 2 groups were significantly higher (n P < 0.05). Compared with the control group, the expression levels of GPx1 protein in L-02 cells of 10 and 20 μmol/L NaAsO n 2 groups were decreased (n P < 0.05). Compared with the control group, the expression levels of Nrf2 protein in L-02 nucleus in 10 and 20 μmol/L NaAsO n 2 groups were significantly increased (n P < 0.05); the expression level of NQO1 protein in L-02 nucleus in 5 μmol/L NaAsO n 2 group was significantly increased (n P < 0.05).n Conclusion:NaAsOn 2 has an effect on the expression of Nrf2 signaling pathway related factors in L-02 cells, and the mechanism of oxidative damage caused by NaAsOn 2 in L-02 cells may be related to Nrf2 signaling pathway.n