Erythropoietin improves oxidative stress following spinal cord trauma in rats

SummarySpinal cord injury (SCI) is a very destructive process for both patients and society. Lipid peroxidation is the main cause of the further secondary damage which starts after mechanical destruction of tissues. Recent studies have shown that erythropoietin (EPO) has neuroprotective properties. In this study, we aimed to see the effect of EPO treatment after spinal cord injury on the oxidant and anti-oxidant enzyme systems and the relationship with the N-methyl-d-Aspartate (NMDA) blockage. Spinal cord injury was produced by epidural compression with a cerebral vascular clip that has a closing force of 40 g for 30 s after a limited multilevel laminectomy (T9-11). Experiment was done in 5 groups: Group1: Sham-operated untraumatised, Group 2: SCI untreated, Group 3: 150 i.u./kg EPO injected i.p. at the end of the first hour following the trauma. Group 4: NMDA receptor antagonist ketamine (100 mg/kg) i.p. Group 5: EPO + ketamine i.p. The experiments were finished after 12 h of the trauma. The spinal cords were excised for biochemical examinations.Anti-oxidant enzymes; catalase and reduced glutathione (GSH) levels increased and lipid peroxidation product, malonyldialdehyde (MDA) level decreased in EPO treated group when compared to the other groups. TNF-α levels decreased in EPO treated group. Application of ketamine before EPO treatment decreased effects of EPO. In conclusion, our results suggest that 150 i.u./kg i.p. EPO, a therapeutic dose in anaemic patients, applied after 1 h of spinal cord injury significantly attenuated the oxidative damage of spinal cord injuries in rats. This activity is abolished via ketamine pretreatment.