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

Abstract 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...

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Veröffentlicht in:Surgical neurology 2008-11, Vol.70 (5), p.498-502
Hauptverfasser: Okutan, Ozerk, MD, Turkoglu, Omer Faruk, MD, Gok, Hayriye Beril, MD, Beskonakli, Etem, MD, PhD
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container_issue 5
container_start_page 498
container_title Surgical neurology
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creator Okutan, Ozerk, MD
Turkoglu, Omer Faruk, MD
Gok, Hayriye Beril, MD
Beskonakli, Etem, MD, PhD
description Abstract 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°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.
doi_str_mv 10.1016/j.surneu.2007.07.061
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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°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.</description><identifier>ISSN: 0090-3019</identifier><identifier>EISSN: 1879-3339</identifier><identifier>DOI: 10.1016/j.surneu.2007.07.061</identifier><identifier>PMID: 18291472</identifier><identifier>CODEN: SGNRAI</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Apoptosis ; Biological and medical sciences ; Blood-brain barrier ; Blood-Brain Barrier - metabolism ; Brain Edema - etiology ; Brain Edema - metabolism ; Brain Edema - prevention &amp; control ; Brain Injuries - complications ; Brain Injuries - drug therapy ; Brain Injuries - pathology ; Caspase ; Caspase 3 - metabolism ; Cold Temperature ; Dexamethasone - therapeutic use ; Disease Models, Animal ; Erythropoietin ; Erythropoietin - therapeutic use ; Glucocorticoids - therapeutic use ; Inflammation ; Male ; Medical sciences ; Myeloperoxidase ; Neurology ; Neuroprotection ; Neurosurgery ; Peroxidase - metabolism ; Rats ; Rats, Sprague-Dawley ; Surgery ; Surgery (general aspects). Transplantations, organ and tissue grafts. 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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°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.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Blood-brain barrier</subject><subject>Blood-Brain Barrier - metabolism</subject><subject>Brain Edema - etiology</subject><subject>Brain Edema - metabolism</subject><subject>Brain Edema - prevention &amp; control</subject><subject>Brain Injuries - complications</subject><subject>Brain Injuries - drug therapy</subject><subject>Brain Injuries - pathology</subject><subject>Caspase</subject><subject>Caspase 3 - metabolism</subject><subject>Cold Temperature</subject><subject>Dexamethasone - therapeutic use</subject><subject>Disease Models, Animal</subject><subject>Erythropoietin</subject><subject>Erythropoietin - therapeutic use</subject><subject>Glucocorticoids - therapeutic use</subject><subject>Inflammation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myeloperoxidase</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neurosurgery</subject><subject>Peroxidase - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Surgery</subject><subject>Surgery (general aspects). 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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°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.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>18291472</pmid><doi>10.1016/j.surneu.2007.07.061</doi><tpages>5</tpages></addata></record>
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subjects Animals
Apoptosis
Biological and medical sciences
Blood-brain barrier
Blood-Brain Barrier - metabolism
Brain Edema - etiology
Brain Edema - metabolism
Brain Edema - prevention & control
Brain Injuries - complications
Brain Injuries - drug therapy
Brain Injuries - pathology
Caspase
Caspase 3 - metabolism
Cold Temperature
Dexamethasone - therapeutic use
Disease Models, Animal
Erythropoietin
Erythropoietin - therapeutic use
Glucocorticoids - therapeutic use
Inflammation
Male
Medical sciences
Myeloperoxidase
Neurology
Neuroprotection
Neurosurgery
Peroxidase - metabolism
Rats
Rats, Sprague-Dawley
Surgery
Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases
title Neuroprotective effect of erythropoietin after experimental cold injury–induced vasogenic brain edema in rats
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