Aim:Cerebrolysin is a well-known neuroprotective agent. This study investigated its effects on inflammation, oxidative stress, apoptosis, and neurologic recovery in the setting of spinal cord ischemia/reperfusion injury (SCIRI) in an experimental animal model.Material and Methods:Rabbits were randomly divided into five groups: control, ischemia, vehicle, methylprednisolone (30 mg/kg), and cerebrolysin (5 ml/kg) group. The rabbits in the control group underwent laparotomy; the other groups underwent spinal cord ischemia and reperfusion injury for 20 min. Neurologic examination after 24 h was based on the Modified Tarlov scale. Myeloperoxidase activities, catalase and malondialdehyde levels, and caspase-3 concentrations were determined in serum and tissue samples. Serum xanthine oxidase levels were studied and histopathological and ultrastructural changes were examined.Results:After SCIRI, serum and tissue myeloperoxidase activities, malondialdehyde levels, caspase-3 concentrations, and serum xanthine oxidase activities were increased (p<0.01–0.001). Catalase levels were significantly diminished (p<0.001). Cerebrolysin treatment correlated with reduced myeloperoxidase and xanthine oxidase activities, malondialdehyde levels and caspase-3 concentrations; and with increased catalase levels (p < 0.001, for all). The cerebrolysin group showed improved histopathological, ultrastructural, and neurological outcomes.Conclusion:For the first time in the literature the current study reports anti-inflammatory, antioxidant, antiapoptotic, and neuroprotective effects of cerebrolysin in a SCIRI rabbit model.