• Ozerk Okutan, Omer Faruk Turkoglu, Hayriye Beril Gok, and Etem Beskonakli.
• Department of Neurosurgery, Ankara Ataturk Research and Education Hospital, Ankara, Turkey. ozerkokutan@hotmail.com
• Surg Neurol. 2008 Nov 1;70(5):498-502.

BackgroundThe aims of this study were to evaluate the efficiency of EPO in the treatment of cold injury-induced brain edema, apoptosis, and inflammation and to compare its effectiveness with DSP.MethodsOne hundred fifteen adult male Sprague-Dawley rats weighing between 280 and 300 g were used for the study. Rats were divided into 5 groups. Controls received craniotomy only. The injury group underwent cold injury and had no medication. In the EPO group, a single dose of 1000 IU/kg body weight of EPO was administered. The DSP group received 0.2 mg/kg body weight of DSP. The vehicle group received a vehicle solution containing human serum albumin, which is the solvent for EPO. Brain edema was formed by cold injury using metal sterile rods with a diameter of 4 mm that were previously cooled at -80 degrees C. Twenty-four hours after the injury, animals were decapitated and brain tissues were investigated for brain edema, tissue MPO and caspase-3 levels, and ultrastructure.ResultsA significant increase in brain water content was revealed in injury group of rats at 24 hours after cold injury. Injury significantly increased tissue MPO and caspase-3 levels and resulted in ultrastructural damage. Both EPO and DSP markedly decreased tissue MPO and caspase-3 levels and preserved ultrastructure of the injured brain cortex.ConclusionsErythropoietin and DSP were found to be neuroprotective in cold injury-induced brain edema model in rats via anti-apoptotic and anti-inflammatory actions.

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