OBJECTIVE To investigate the protective effects of Naodesheng Effective Composite (NEC) on PC12 cells apoptosis induced by H2O2 and mitochondria injury induced by Fe2 +-cysteine system.METHODS To study the effects of NEC (1, 10, 100 μg·ml-1) on H2O2 exposed to PC12 cells, cells were pretreated with NEC or without NEC for 4 h followed by 200 μmol· L-1 H2O2 for 12 h.Cell viability was measured by MTT assay.The chromatin-specific dye Hoechst 33342 was used to observe nuclear changes.Caspase-3 activity was detected with a protease assay using Ac-DEVD-AMC as a substrate.Cytochrome c expression was determined by western blotting.Furthermore, the protection of NEC on Fe2 +-cysteine system-induced rat brain mitochondriai injury was observed.Mitochondrial swelling degree was detected based on turbidity changes.Mitochondrial membrane potential was assayed based on the intake of Rhodamin 123.Malondialdehyde (MDA) content was determined by the reaction of MDA with thiobartituric acid to form the chronophoric products.Activity of glutathione peroxidase (GSH) was determined by measuring the disappearance of NADPH.RESULTS Following exposure of PC12 cells to H2O2, there was a significant reducing in PC12 cells survival, in contrast, the increased levels in the leakage of lactate dehydrogenase (LDH), caspase-3 activity, release of cytochrome c to cytosol.In addition, Fe2+-cysteine system induced increasing of rat brain mitochondria swelling, membrane potential, MDA content except for reducing GSH content.However, pretreatment of NEC attenuated all the changes.CONCLUSION All of these results suggest NEC has the neuroprotective capacity to antagonize oxide stress-induced apoptosis, which partially was associated with inhibition of caspase activity, decrease of cytochrome c release, and improvement of mitochondrial functions.