摘要
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。
Objective To study the role of hydrogen peroxide on curcurnin induced apoptosis of hepatocellular carcinoma. Methods Curcumin or curcumin combined with catalase acted on hepatoeellular 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）%0 after 24,48h（P〈0.01）. Catalase could reduce these changes（P〈0.01）. Conclusion Curcumin in time dependent way induced hepa-tocelllar carcinoma apoptosis by ascending hydrogen peroxide which damaged mitochondrial membrane potential.
出处
《重庆医学》
CAS
CSCD
北大核心
2012年第3期269-270,274,共3页
Chongqing medicine
关键词
姜黄素
过氧化氢
线粒体膜电位
凋亡
curcumin
hydrogen peroxide
mitochondrial membrane potential
apoptosis
