PX-12通过氧化应激诱导肝癌细胞凋亡的作用机制

Mechanism of PX-12 induced apoptosis of hepatocellular carcinoma cells through oxidative stress

目的:探究PX-12诱导肝癌细胞凋亡的作用机制。方法:选取人肝癌细胞株Huh7作为主要研究对象,采用硫氧还蛋白抑制剂PX-12处理细胞后,CCK8法检测细胞活力,细胞划痕实验检测细胞的迁移能力,细胞增殖试剂盒检测细胞增殖能力,流式细胞术检测细胞内活性氧水平和凋亡水平,Westernblot检测凋亡相关蛋白表达变化。结果:与对照组相比,PX-12处理组的细胞活力、迁移能力和增殖能力都显著下降(P<0.05),细胞内活性氧水平升高(P<0.05),且呈浓度依赖性。凋亡抑制剂Z-VAD-FMK和抗氧化剂NAC能恢复其细胞活力,并且NAC能降低PX-12引起的细胞内活性氧的积累,恢复PX-12诱导的细胞凋亡(P<0.05)。结论:PX-12通过氧化应激的方式诱导肝癌细胞发生凋亡。

AIM:To explore the mechanism of PX-12 induced apoptosis of hepatocellular carcinoma cells.METHODS:Human hepatoma cell line Huh7 was selected as the main research object.After the cells were treated with thioredoxin inhibitor PX-12,the cell viability was detected by CCK8 method,the cell migration ability was detected by cell scratch test,the cell proliferation ability was detected by cell proliferation kit,the levels of intracellular reactive oxygen species and apoptosis were detected by flow cytometry,and the expression of apoptosis-related proteins were detected by Western blot.RESULTS:Compared with the control group,the cell viability,migration ability and proliferation ability of PX-12 treatment group were significantly decreased(P<0.05),and the level of intracellular reactive oxygen species was increased(P<0.05)in a concentration dependent manner.Apoptosis inhibitor Z-VAD-FMK and antioxidant NAC could restore the cell viability,and NAC could reduce the accumulation of intracellular reactive oxygen species induced by PX-12 and restore the apoptosis induced by PX-12(P<0.05).CONCLUSION:PX-12 induces apoptosis of hepato-cellular carcinoma cells through oxidative stress.