首页|PX-12通过氧化应激诱导肝癌细胞凋亡的作用机制

PX-12通过氧化应激诱导肝癌细胞凋亡的作用机制

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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,Western blot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。
Mechanism of PX-12 induced apoptosis of hepatocellular carcinoma cells through oxidative stress
AIM:To explore the mechanism of PX-12 induced apoptosis of hepatocellular carcinoma cells.METHODS:Human hepatoma cell line Huh7 was se-lected 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 mi-gration ability was detected by cell scratch test,the cell proliferation ability was detected by cell prolif-eration kit,the levels of intracellular reactive oxygen species and apoptosis were detected by flow cy-tometry,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 intracel-lular 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.

hepatocellular carcinomaPX-12oxi-dative stressapoptosis

雷国杰、于艳华、刘影超、边文霞、杜璟、童向民

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浙江中医药大学,杭州 310053,浙江

浙江省人民医院(附属人民医院),杭州医学院,检验中心,杭州 310006,浙江

杭州市第一人民医院血液科,杭州 310006,浙江

肝癌 PX-12 氧化应激 凋亡

国家自然科学基金资助项目

82102938

2024

中国临床药理学与治疗学
中国药理学会

中国临床药理学与治疗学

CSTPCD北大核心
影响因子:0.97
ISSN:1009-2501
年,卷(期):2024.29(9)