柯里拉京对人肺癌细胞A549的抑制作用及其机制研究

Inhibitory Effects of Corilagin on Human Lung Cancer Cell A549 and the Underlying Mechanism

该研究旨在探讨柯里拉京对人肺癌A549细胞凋亡的影响及其潜在作用机制。采用CCK-8细胞活性检测试剂盒检测柯里拉京对A549细胞活性的影响;通过流式细胞术检测细胞凋亡;JC-1线粒体膜电位检测试剂盒检测线粒体膜电位;免疫印迹法检测凋亡相关蛋白(bax、bcl-2、cleaved-caspase-3、cleaved-PARP)的表达量;通过DCFH-DA探针标记检测细胞内ROS水平。研究结果显示,柯里拉京处理能够剂量依赖性地抑制A549细胞的活性,并通过上调bax的表达、下调bcl-2的表达,破坏线粒体膜电位,促进有活性的cleaved-caspase-3以及cleaved-PARP的形成,诱导A549细胞凋亡。活性氧清除剂NAC能够明显逆转柯里拉京诱导的细胞凋亡。因此,柯里拉京可能通过调节胞内ROS水平诱导人肺癌细胞A549发生凋亡。

The aim of this study was to explore the influences of corilagin on the apoptosis of A549 cells and the underlying action mechanism.The cell viability of A549 cells was detected by CCK-8 assay kit.The apoptosis was analyzed by flow cytometry.The mitochondrial membrane potential was detected by JC-1 assay kit.The expression levels of apoptotic proteins(bax,bcl-2,cleaved-caspase-3 and cleaved-PARP)were detected by Western blot.The ROS levels were evaluated by DCFH-DA probe labeling.The results showed that corilagin dose-dependently inhibited cell viability,and it could up-regulate bax and down-regulate bcl-2.Then,mitochondrial membrane potential was damaged,and the formation of active cleaved-caspase-3 and cleaved-PARP were promoted,finally inducing apoptosis of A549 cells.NAC(a ROS scavenger)could obviously reverse corilagin-induced apoptosis.Therefore,corilagin may induce the apoptosis of human lung cancer A549 cells by regulating intracellular ROS levels.