Background: Edaravone had been validated to effectively protect against ischemic injuries. In this study, we inves- tigated the protective effect of edaravone by observing the effects on anti-apoptosis, regulation of Bcl-2/Bax protein expression and recovering from damage to mitochondria after OGD (oxygen-glucose deprivation)-reperfusion. Methods: Viability of PC12 cells which were injured at different time of OGD injury, was quantified by measuring MTT (2-(4,5-dimethylthia- zol-2-yl)-2,5-diphenyltetrazolium bromide) staining. In addition, PC12 cells’ viability was also quantified after their preincubation in different concentration of edaravone for 30 min followed by (OGD). Furthermore, apoptotic population of PC12 cells that reinsulted from OGD-reperfusion with or without preincubation with edaravone was determined by flow cytometer analysis, electron microscope and Hoechst/PI staining. Finally, change of Bcl-2/Bax protein expression was detected by Western blot. Results: (1) The viability of PC12 cells decreased with time (1~12 h) after OGD. We regarded the model of OGD 2 h, then re- placing DMEM (Dulbecco’s Modified Eagle’s Medium) for another 24 h as an OGD-reperfusion in this research. Furthermore, most PC12 cells were in the state of apoptosis after OGD-reperfusion. (2) The viability of PC12 cells preincubated with edaravone at high concentrations (1, 0.1, 0.01 μmol/L) increased significantly with edaravone protecting PC12 cells from apoptosis after OGD-reperfusion injury. (3) Furthermore, edaravone attenuates the damage of OGD-reperfusion on mitochondria and regulated Bcl-2/Bax protein imbalance expression after OGD-reperfusion. Conclusion: Neuroprotective effects of edaravone on ischemic or other brain injuries may be partly mediated through inhibition of Bcl-2/Bax apoptotic pathways by recovering from the damage of mitochondria. Background: Edaravone had been validated to effectively protect against ischemic injuries. In this study, we inves- tigated the protective effect of edaravone by observing the effects on anti-apoptosis, regulation of Bcl-2 / Bax protein expression and recovering from damage to mitochondria after OGD (oxygen-glucose deprivation) -reperfusion. Methods: Viability of PC12 cells which were injured at different time of OGD injury, was quantified by MTT (2- (4,5-dimethylthia- zol- , 5-diphenyltetrazolium bromide). In addition, PC12 cells’ viability was also quantified after their preincubation in different concentrations of edaravone for 30 min followed by (OGD). Further, apoptotic population of PC12 cells that reinsulted from OGD-reperfusion with or Without preincubation with edaravone was determined by flow cytometer analysis, electron microscope and Hoechst / PI staining. Finally, change of Bcl-2 / Bax protein expression was detected by Western blot. Results: (1) The v We considered the model of OGD 2 h, then re-placing DMEM (Dulbecco’s Modified Eagle’s Medium) for another 24 h as an OGD-reperfusion in this research. iability of PC12 cells decreased with time (1 ~ 12 h) after OGD. , most PC12 cells were in the state of apoptosis after OGD-reperfusion. (2) The viability of PC12 cells preincubated with edaravone at high concentrations (1, 0.1, 0.01 μmol / L) increased significantly with edaravone protecting PC12 cells from apoptosis after OGD -reperfusion injury. (3) Further, edaravone attenuates the damage of OGD-reperfusion on mitochondria and regulated Bcl-2 / Bax protein imbalance expression after OGD-reperfusion. Conclusion: Neuroprotective effects of edaravone on ischemic or other brain injuries may be partly mediated through inhibition of Bcl-2 / Bax apoptotic pathways by recovering from the damage of mitochondria.