Inhibition by epigallocatechin gallate of CoCl2-induced apoptosis in rat PC12 cells

Abstract Epigallocatechin-3-gallate (EGCG) is a major constituent of green tea polyphenols. This study was aimed to investigate the possible mechanisms of EGCG-mediated inhibition against apoptosis in rat pheochromocytoma PC12 cells by exposure to CoCl 2 . Exposure to CoCl 2 caused the generation of ROS and induced cell death with appearance of apoptotic morphology and DNA fragmentation. However, EGCG rescued the loss of viability in the cells exposed to CoCl 2 and led the reduction of DNA fragmentation and sub-G 1 fraction of cell cycle. Also, EGCG attenuated the CoCl 2 -induced disruption of mitochondrial membrane potential (ΔΨm), release of cytochrome c from the mitochondria to cytosol and abolished the CoCl 2 -stimulated activities of the caspase cascades, caspase-9 and caspase-3. In addition, EGCG ameliorated the increase in the Bax to Bcl-2 ratio, a marker of apoptosis proceeding, induced by CoCl 2 treatment. Taken together, the present results suggest that EGCG inhibit the CoCl 2 -induced apoptosis of PC12 cells through the mitochondria-mediated apoptosis pathway involved in modulating the Bcl-2 family.