Abstract

Anticancer effects of corosolic acid have been demonstrated earlier in human cervix adenocarcinoma and osteosarcoma cells, but the exact underlying molecular mechanisms have not been studied. Hence, an attempt was made to identify the anticancer mechanism of corosolic acid in human hepatocellular carcinoma cells [HepG2]. The anticancer activity of corosolic acid through cell growth inhibition by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, reactive oxygen species (ROS) generation, mitochondrial membrane potential and apoptotic fragmentations by fluorescence microscope was evaluated. In addition, the cleavage of PARP, NF-κB, cytochrome c (cyt. C) release, and Bax and Bcl2 expression was analyzed by Western blot. The results clearly indicate that corosolic acid was involved in the alteration of mitochondrial membrane potential resulting in the release of cyt. Cfrom mitochondria and increased ROS generation. The corosolic acid treatment causes the induction of apoptosis in a dose dependent manner (IC_50, 40 µM). In conclusion, corosolic acid had chemopreventive effect on HepG2 cells by apoptosis.

Key words: Corosolic acid, hepatocellular carcinoma, reactive oxygen species (ROS), apoptosis, lipid peroxidation.