Chrysophanol Stimulates Mitochondrial-Dependent Cell Apoptosis via ROS and Inhibits NF-κB Signaling in Cervical Cancer Cells

Chrysophanol (CHR) is a secondary metabolite of anthraquinone class and several studies have documented the potential therapeutic features of chrysophanol in modulating the number of signaling pathways associated with cell proliferation and apoptosis. Present study was concerned to examine the efficiency of chrysophanol on cell viability, reactive oxygen species (ROS) and mechanism to stimulate the anti and pro-apoptosis related Bcl-2 and Bax family proteins, caspases 3 and 9 related mitochondrial mediated intrinsic apoptotic pathway and the nuclear factor kappa-B (NF-kappa B) signaling in cervical cancer cells. The results of this study explored that CHR apparently produce excessive reactive oxygen species (ROS) thereby made the mitochondrial membrane depolarization, in cervical cancer cells and stimulating apoptosis and suppressing NF-kappa B activity. We suggested that CHR exhibits great potential in stimulating the apoptosis of cervical cancer cells and proposed to be ideal bioactive molecule for cervical cancer therapy.