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. The gene discussed is HIF1A; the disease is brain ischemia.