硒诱导HepG2细胞凋亡与活性氧的关系

目的探讨亚硒酸钠(Na2SeO3)诱导细胞凋亡的可能作用机制。方法用0、2.5、5、10和20μmol/L的Na2SeO3以及加有N-乙酰基-L-半胱氨酸(NAC)的Na2SeO3(10μmol/L)处理HepG2。用四甲基偶氮唑盐(MTT)比色法测定细胞活性;流式细胞仪测细胞内活性氧(ROS)的水平以及细胞凋亡情况。结果5、10和20μmol/LNa2SeO3作用于HepG21h即引起ROS增加,12h后HepG2细胞活性降低,24h后细胞早期凋亡以及晚期凋亡/坏死率均增加,与对照组相比差异有显著性(P<0.05);抗氧化剂NAC有效抑制了ROS的增加,并增加了细胞活性,降低了细胞凋亡率,与未加NAC的Na2SeO3组(10μmol/L)相比差异有显著性(P<0.05)。结论一定浓度的亚硒酸钠使HepG2细胞活性下降,促进了细胞凋亡,ROS的增加在其中发挥了作用。

Relationship between reactive oxygen species and apoptosis in HepG2 cells induced by sodium selenite

OBJECTIVE: To investigate the mechanism of sodium selenite-induced apoptosis in HepG2 cells. METHODS: HepG2 cells were treated with 0,2.5,5,10 and 20 micromol/L sodium selenite for different time, and NAC (5 micromol) was added simultaneously with selenite (10 micromol/L). Then the cell viability was detected by MTT, and the fluorescent intensity of ROS and the apoptosis rate was determined by flow cytometry. RESULTS: Compared with the control group, the levels of ROS were increased after HepG2 was treated with 5, 10 and 20 micromol/L sodium selenite for one hour, and the cell viability decreased after 12 hours, and the apoptosis rate of HepG2 was increased. After NAC was added with selenite, ROS was effectively inhibited. Subsequently cell viability was increased and the cell apoptosis rate was decreased. CONCLUSION: ROS may play a crucial role in sodium selenite-decreased cell viability and -induced apoptosis in HepG2 cells.