• Ataç Sönmez, Birol Kabakçi, Enver Vardar, Duygu Gürel, Ulker Sönmez, Yahya T Orhan, Unal Açikel, and Necati Gökmen.
• Learning Resources Center Research Laboratory, School of Medicine, Dokuz Eylul University Inciralti, TR-35340, Izmir, Turkey. atac.sonmez@deu.edu.tr
• Surg Neurol. 2007 Sep 1; 68 (3): 297-303; discussion 303.

BackgroundRecent studies have suggested that EPO activates the CREB transcription pathway and increases BDNF expression and production, which contributes to EPO-mediated neuroprotection. We investigated whether EPO has a neuroprotective effect against ISCI in rats and examined the involvement of CREB protein phosphorylation in this process.MethodsSpinal cord ischemia was produced by balloon occlusion of the abdominal aorta below the branching point of the left subclavian artery for 5 minutes, and rHu-EPO (1000 U/kg BW) was administered intravenously after the onset of the reperfusion. Neurologic status was assessed at 1, 24, and, 48 hours. After the end of 48 hours, spinal cords were harvested for histopathologic analysis and immunohistochemistry for pCREB.ResultsAll sham-operated rats had a normal neurologic outcome, whereas all ischemic rats suffered severe neurologic deficits after ISCI. Erythropoietin treatment was found to accelerate recovery of motor deficits and prevent the loss of motoneurons in the spinal cord after transient ischemia. Ischemic spinal cord injury induced the phosphorylation of pCREB at the anterior horn of the spinal cord, and EPO treatment significantly potentiated expression of pCREB increase at the anterior horn of the spinal cord.ConclusionsThese results demonstrate that a single dose of EPO given before ISCI provides significant neuroprotection and potentiates the expression of pCREB in this region.

24 keywords...

hide…