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

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 CoCl2. Exposure to CoCl2 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 CoCl2 and led the reduction of DNA fragmentation and sub-G1 fraction of cell cycle. Also, EGCG attenuated the CoCl2-induced disruption of mitochondrial membrane potential (ΔΨm), release of cytochrome c from the mitochondria to cytosol and abolished the CoCl2-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 CoCl2 treatment. Taken together, the present results suggest that EGCG inhibit the CoCl2-induced apoptosis of PC12 cells through the mitochondria-mediated apoptosis pathway involved in modulating the Bcl-2 family.