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

ZHANG Ping¹, LI Xinyuan², ZHA Qingbing³^*

(¹Clinical Medical Laboratory Center, the First Affiliated Hospital of Jinan University, Guangzhou 510630, China; ²Clinical Medicine, School of Basic Medicine, Jinan University, Guangzhou 510632, China; ³Department of Fetal Medicine, the First Affiliated Hospital of Jinan University, Guangzhou 510630, China)

Abstract:

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.

CSTR: 32200.14.cjcb.2020.09.0004