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目的:探讨姜黄素损伤线粒体诱导食管癌Ec-109细胞凋亡的作用机制。方法:80μmol/mL姜黄素作用于食管癌Ec-109细胞不同时间后,流式细胞仪检测细胞亚二倍体凋亡峰变化及线粒体膜电位变化;蛋白质印迹法检测细胞色素C释放及Caspase-9表达。结果:姜黄素呈时间依赖性诱导食管癌Ec-109细胞凋亡,12、24和48 h细胞亚二倍体凋亡峰分别为(15.89±2.12)%、(26.80±1.87)%和(36.97±1.80)%,对照组为(3.23±0.24)%,总体比较差异有统计学意义,F=6.75,P<0.01,各组间比较差异均有统计学意义,P<0.01。姜黄素作用3、6和12 h后线粒体膜电位分别为84.78%、67.03%和63.16%,对照组为97.17%,差异有统计学意义,F=5.12,P<0.05,各组间比较,6 h组与12 h组差异无统计学意义,P=0.062,余各组间有差别;6 h出现细胞色素C表达,12 h表达最高;12 h检测到Caspase-9表达,24 h表达最高。结论:姜黄素呈时间依赖性诱导食管癌细胞凋亡是通过损伤细胞线粒体、使之释放出细胞色素C以及激活Caspase-9实现的。
Objective: To investigate the mechanism of curcumin on mitochondria-induced esophageal cancer Ec-109 cells apoptosis. Methods: After treated with 80μmol / mL curcumin for different times, the apoptotic changes of sub-diploid cells and mitochondrial membrane potential were detected by flow cytometry. The expressions of cytochrome C and Caspase- 9 expression. RESULTS: Curcumin induced the apoptosis of EC-109 cells in a time-dependent manner. The apoptotic peaks of sub-diploid cells at 12, 24 and 48 h were (15.89 ± 2.12)%, (26.80 ± 1.87)% and (36.97 ± 1.80)% in the control group and (3.23 ± 0.24)% in the control group. The overall difference was statistically significant (F = 6.75, P <0.01). There was significant difference among the groups (P <0.01). The mitochondrial membrane potential of curcumin at 3, 6 and 12 h were 84.78%, 67.03% and 63.16%, respectively, and the control group was 97.17%, the difference was statistically significant (F = 5.12, P <0.05) There was no significant difference between h group and 12 h group (P = 0.062). There were differences among the groups. Cytochrome C expression was found at 6 h and highest at 12 h. Caspase-9 expression was detected at 12 h and highest at 24 h. CONCLUSION: Curcumin induces apoptosis in esophageal cancer cells in a time-dependent manner by damaging the mitochondria, releasing cytochrome C and activating Caspase-9.