山杏叶乙酸乙酯提取物调控乳腺癌MCF7细胞增殖和凋亡的机制研究

为探究山杏叶乙酸乙酯提取物对乳腺癌MCF7细胞株增殖和凋亡的影响,本研究采用CCK8法检测山杏叶提取物对MCF7细胞增殖的抑制作用,流式细胞仪检测细胞凋亡率,倒置荧光显微镜和流式细胞仪分别检测胞内活性氧(ROS)的水平变化,RT-PCR检测细胞周期及凋亡相关基因的表达情况,试剂盒检测caspase-3的活性。实验表明,山杏叶提取物可降低MCF7细胞存活率,促进细胞凋亡,增加胞内ROS水平。同时上调和Bax,下调Bcl-2,增强caspase-3活性,并降低CDK4、CyclinE和CyclinD1的表达。综上说明山杏叶提取物可通过调控周期蛋白的表达来抑制MCF7细胞的增殖,并通过caspase途径和提升ROS水平来诱导MCF7细胞的凋亡。

Mechanism of proliferation and apoptosis in breast cancer cells MCF7 induced by ethyl acetate extract of wild apricot leaves

To explore the effect of ethyl acetate extract of wild apricot leaves on proliferation and apoptosis of breast cancer MCF7 cell,CCK8 assay was used to detect the inhibitory effect of extract of wild apricot leaves on the proliferation of MCF7 cells.Flow cytometry was used to detect the apoptosis rate.Inverted fluorescence microscopy and flow cytometry were used to detect the changes of intracellular reactive oxygen species (ROS).RT-PCR was used to detect the expression of cell cycle and apoptosis-related genes.Detection kit was used to measure caspase-3 activity.The results showed that extract of wild apricot leaves could reduce the survival rate of MCF7 cells,promote cell apoptosis and increase the level of intracellular reactive oxygen species (ROS).Further,it could up-regulate Bax,down-regulate Bcl-2,enhance caspase-3 activity,and reduce the expression of CDK4,Cyclin E and Cyclin D1.In conclusion,ethyl acetate extract of wild apricot leaves could inhibit the proliferation of MCF7 cells by regulating cyclin expressions,and induce apoptosis of MCF7 by caspase pathway and the up-regulating of ROS level.