BACKGROUND: The 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. METHODS: One 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. RESULTS: A 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. CONCLUSIONS: Erythropoietin and DSP were found to be neuroprotective in cold injury-induced brain edema model in rats via anti-apoptotic and anti-inflammatory actions.
BACKGROUND: The 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. METHODS: One 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. RESULTS: A 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. CONCLUSIONS:Erythropoietin and DSP were found to be neuroprotective in cold injury-induced brain edema model in rats via anti-apoptotic and anti-inflammatory actions.
Authors: Michael Brines; Nimesh S A Patel; Pia Villa; Courtenay Brines; Tiziana Mennini; Massimiliano De Paola; Zubeyde Erbayraktar; Serhat Erbayraktar; Bruno Sepodes; Christoph Thiemermann; Pietro Ghezzi; Michael Yamin; Carla C Hand; Qiao-wen Xie; Thomas Coleman; Anthony Cerami Journal: Proc Natl Acad Sci U S A Date: 2008-08-01 Impact factor: 11.205