In conclusion, using a model of transient cerebral ischemia and hypoxic culture of NSPCs, we found that pre- and postadministration of edaravone mitigated hippocampal CA1 injury and enhanced neurogenesis by protecting NSPCs from apoptosis, which was probably mediated by decreasing ROS generation and inhibiting protein expressions of HIF-1α and cleaved caspase-3 after cerebral ischemia. Here, CASP3 is linked to transient ischemic attack.