论文部分内容阅读
目的观察二甲基甲酰胺(DMF)对HL7702肝细胞的细胞活力、凋亡及线粒体膜电位的影响,探讨DMF引起肝细胞凋亡的可能机制。方法 HL7702肝细胞给予50、100、150、200和250 mmol/L DMF处理,于24 h后检测其细胞存活率,乳酸脱氢酶(LDH)释放量。根据细胞毒性测试结果设置对照组及DMF染毒组(200 mmol/L)。流式细胞术检测DMF对HL7702细胞凋亡以及对线粒体膜电位的影响。结果 DMF剂量依赖性地降低HL7702细胞的存活率,其中150、200和250 mmol/L DMF组与对照组相比,细胞存活率明显降低;并且,随着DMF染毒浓度增加,释放至细胞外的LDH的含量增加,与DMF浓度呈正相关。200 mmol/L DMF染毒24 h后,与对照组相比,细胞凋亡率增加,差异有统计学意义(P<0.001),线粒体膜电位降低,差异也有统计学意义(P<0.001)。结论 DMF对HL7702细胞的毒性作用具有剂量依赖性,DMF引起HL7702线粒体膜电位的改变与DMF导致细胞凋亡有关。
Objective To observe the effect of dimethylformamide (DMF) on the cell viability, apoptosis and mitochondrial membrane potential of HL7702 hepatocytes and to explore the possible mechanism of DMF induced apoptosis in hepatocytes. Methods HL7702 hepatocytes were treated with 50, 100, 150, 200 and 250 mmol / L DMF. After 24 h, the cell viability and lactate dehydrogenase (LDH) release were measured. The control group and DMF-treated group (200 mmol / L) were set according to the cytotoxicity test results. Flow cytometry was used to detect the apoptosis of HL7702 cells and its effect on mitochondrial membrane potential. Results DMF dose-dependently reduced the survival rate of HL7702 cells, and the cell survival rates of 150, 200 and 250 mmol / L DMF groups were significantly decreased compared with the control group; and, with the increase of DMF concentration, the release to extracellular Of the LDH content increased, and DMF concentration was positively correlated. Compared with the control group, the apoptosis rate increased after 200 mmol / L DMF exposure for 24 h (P <0.001), and the mitochondrial membrane potential decreased (P <0.001). Conclusion The toxic effects of DMF on HL7702 cells in a dose-dependent manner, DMF-induced HL7702 mitochondrial membrane potential changes associated with DMF-induced apoptosis.