中文摘要：

目的观察亚砷酸钠染毒对人肝细胞（L02）凋亡及其机制的探讨。方法采用人肝细胞L02细胞株,亚砷酸钠染毒剂量范围为0~40μmol/L,处理时间为24和48 h。MTT法检测细胞增殖,并将活力为80%以上作为染毒剂量,选择亚砷酸钠终浓度为0、1.0、5.0和10μmol/L,处理24h。Hochest33258染色法观察细胞凋亡,CM-H2DCFDA荧光染色法观察胞内ROS形成,Western bloting检测NF-κB信号通路p-p65及p65蛋白的表达,用NAC干预2 h,加亚砷酸钠5.0μmol/L处理后,进一步观察上述指标。结果随着砷染毒剂量的增加,细胞增殖呈现先增高后降低的趋势,凋亡细胞数和胞内ROS则呈现逐步增多的现象,但NAC预处理后ROS产生及凋亡细胞数目则显著降低,提示氧化应激在砷致人肝细胞L02中发挥作用;p-p65蛋白表达水平随砷染毒剂量的增加而增加,NAC预处理可降低其形成,以上差异均有统计学意义。结论亚砷酸钠可经由氧化应激引起人肝细胞L02发生凋亡,且激活NF-κB信号通路有关。

英文摘要：

Objective To discuss apotosis by sodium arsenite exposure induced observed in L02 cells and its mechanism. Method The L02 cells were used as the target cells. Sodium arsenite exposure dose range was 0 ~ 40 μmol / L,and the treatment time was 24 h and48 h. In order to determine the endothelial cell function upon arsenic exposure,The cell viability was examined by MTT assay. Intracellular ROS production was measured by fluorescent probe CM-H2 DCFDA and apoptosis was measured by fluorescent probe Hochest33258. The core components of NF-κB signaling,including p-p65 and p65 protein level were detemined by using western blotting. Results It was showed that the cell viability increased in 0 ~ 5 μmol / L,but reduced at 20 and 40 μmol / L sodium arsenite. It was observed that arsenic exposure increased apoptosis cells,ROS production and p-p65,and inhibited by adding NAC. These differences were statistically significant.Conclusions Sodium arsenite can induce apoptosis via oridative seress in L02 cells,which involved with the activation of NF-κB signaling pathways.