Neuroprotective effect of erythropoietin after experimental cold injury–induced vasogenic brain edema in rats

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°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.