姜黄素氧化损伤线粒体诱导肝癌SMMC-7721细胞凋亡的研究

目的探讨姜黄素诱导肝癌SMMC-7721细胞凋亡的机制。方法 80μmol/L姜黄素作用于肝癌细胞后,用流式细胞仪检测细胞过氧化氢(H2O2)、线粒体膜电位和细胞亚二倍体凋亡峰情况;比较姜黄素组和预处理组(姜黄素联合过氧化氢酶)线粒体膜电位和细胞亚二倍体凋亡峰变化情况。结果 80μmol/L姜黄素作用于肝癌细胞1、2、3h后检测H2O2分别为(13.49±3.23)%、(52.43±6.04)%、(48.21±7.18)%,以2h时间点最高。细胞线粒体膜电位在6、12h分别为(59.68±4.47)%、(29.83±6.22)%,差异有统计学意义(P<0.01)。细胞亚二倍体凋亡峰在24、48h分别为(26.53±4.28)%、(39.50±6.14)%,差异有统计学意义(P<0.01)。过氧化氢酶均能抑制上述2项指标改变,差异有统计学意义(P<0.05)。结论姜黄素作用肝癌细胞后产生H2O2,H2O2损伤细胞线粒体,呈时间依赖性诱导肝癌细胞凋亡。

Curcumn induced apoptosis of hepatocellular carcinoma by oxidative damaged mitochondria

Objective To study the role of hydrogen peroxide on curcumin induced apoptosis of hepatocellular carcinoma.Methods Curcumin or curcumin combined with catalase acted on hepatocellular carcinoma,hydrogen peroxide,apoptotic Sub-G1 peak and mitochondrial membrane potential were detected by flow cytometer.Results Hydrogen peroxide ascended to(13.49±3.23)%,(52.43±6.04)%,(48.21±7.18)% respectively after 1,2,3 h.Mitochondrial membrane potential was damaged to(59.68±4.47)% and(29.83±6.22)% after 6,12 h(P<0.01).Apoptotic Sub-G1 peak was(26.53±4.28)% and(39.50±6.14)% after 24,48h(P<0.01).Catalase could reduce these changes(P<0.01).Conclusion Curcumin in time dependent way induced hepatocelllar carcinoma apoptosis by ascending hydrogen peroxide which damaged mitochondrial membrane potential.