论文部分内容阅读
目的:研究华蟾素诱导乳腺癌MDA-MB-231细胞凋亡过程中,细胞内活性氧(ROS)及线粒体膜电位(△Ψm)的变化,探讨华蟾素对乳腺癌细胞的作用机制。方法:用不同浓度的华蟾素作用于MDA-MB-231细胞24h后,分别用荧光探针罗丹明123和荧光探针DCFH-DA进行荧光染色,用流式细胞仪检测细胞内线粒体膜电位和活性氧的变化。结果:不同浓度的华蟾素作用于MDA-MB-231细胞后,随着药物浓度的增加(0、12.5、25、37.5、50μg/ml),细胞内的ROS水平显著升高,荧光强度从3 609±24上升为6 263±35;同时,线粒体膜电位(△Ψm)显著下降,荧光强度从242±6降低到173±4。结论:华蟾素作用细胞后,使得细胞内活性氧水平显著升高,同时,线粒体膜电位显著下降,推测华蟾素对MDA-MB-231细胞通过线粒体途径诱发细胞凋亡。
Objective: To study the changes of intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (△ Ψm) in cinobufacini-induced breast cancer MDA-MB-231 cells apoptosis and to explore the mechanism of action of cinobufacini on breast cancer cells. Methods: After treated with different concentrations of cinobufacine for 24 hours, the cells were stained with rhodamine 123 and DCFH-DA respectively. The mitochondrial membrane potential And reactive oxygen species changes. Results: After treated with different concentrations of cinobufacine for MDA-MB-231 cells, the intracellular ROS level increased significantly with the increase of drug concentration (0,12.5,25,37.5,50μg / ml). The fluorescence intensity increased from 3 609 ± 24 increased to 6 263 ± 35. At the same time, mitochondrial membrane potential (△ Ψm) decreased significantly, and fluorescence intensity decreased from 242 ± 6 to 173 ± 4. CONCLUSION: Cinobufacini can increase the level of reactive oxygen species (ROS) in cells and decrease the mitochondrial membrane potential. It is speculated that cinobufacini induced apoptosis of MDA-MB-231 cells through mitochondrial pathway.