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RESEARCH PRODUCT
Neuroprotection by erythropoietin administration after experimental traumatic brain injury.
Alessandra SfacteriaGiovanni GrassoFrancesco MeliDomenico Gerardo IacopinoMichele BuemiVincenzo Fodalesubject
MaleTime FactorsBrain EdemaFunctional LateralityRats Sprague-Dawleychemistry.chemical_compoundTraumatic brain injuryMedicineAnalysis of Variance Animals Blood-Brain Barrier; drug effects Brain Edema; drug therapy/etiology Brain Infarction; drug therapy/etiology Brain Injuries; complications/drug therapy Disease Models; Animal Erythropoietin; administration /&/ dosage Evans Blue; diagnostic use Functional Laterality Humans Male Neurologic Examination Neuroprotective Agents; administration /&/ dosage Rats Rats; Sprague-Dawley Reaction Time; drug effects Recombinant Proteins Time Factorsadministration /&/ dosageSpinal cord injuryEvans BlueNeurologic ExaminationGeneral Neuroscienceexperimental models of brain and spinal cord injuryExtravasationNeuroprotectionRecombinant Proteinsmedicine.anatomical_structureNeuroprotective AgentsBlood-Brain BarrierAnesthesiadiagnostic usemedicine.drugEvans BlueBrain InfarctionTraumatic brain injuryCentral nervous systemrecombinant human EPO (rHuEPO)PlaceboNeuroprotectionReaction TimeAnimalsHumansMolecular BiologyErythropoietinAnalysis of VarianceNeuroscience (all)business.industryAnimaldrug therapy/etiologymedicine.diseaseRatsDisease Models AnimalchemistryErythropoietindrug effectsBrain InjuriesDisease Modelsrecombinant human EPO (rHuEPO); experimental models of brain and spinal cord injury; NeuroprotectionNeurology (clinical)Sprague-Dawleybusinesscomplications/drug therapyDevelopmental Biologydescription
A large body of evidence indicates that the hormone erythropoietin (EPO) exerts beneficial effects in the central nervous system (CNS). To date, EPO's effect has been assessed in several experimental models of brain and spinal cord injury. This study was conducted to validate whether treatment with recombinant human EPO (rHuEPO) would limit the extent of injury following experimental TBI. Experimental TBI was induced in rats by a cryogenic injury model. rHuEPO or placebo was injected intraperitoneally immediately after the injury and then every 8 h until 2 or 14 days. Forty-eight hours after injury brain water content, an indicator of brain edema, was measured with the wet-dry method and blood-brain barrier (BBB) breakdown was evaluated by assay of Evans blue extravasation. Furthermore, extent of cerebral damage was assessed. Administration of rHuEPO markedly improved recovery from motor dysfunction compared with placebo group (P < 0.05). Brain edema was significantly reduced in the cortex of the EPO-treated group relative to that in the placebo-treated group (80.6 ± 0.3% versus 91.8% ± 0.8% respectively, P < 0.05). BBB breakdown was significantly lower in EPO-treated group than in the placebo-treated group (66.2 ± 18.7 μg/g versus 181.3 ± 21 μg/g, respectively, P < 0.05). EPO treatment reduced injury volume significantly compared with placebo group (17.4 ± 5.4 mm3 versus 37.1 ± 5.3 mm3, P < 0.05). EPO, administered in its recombinant form, affords significant neuroprotection in experimental TBI model and may hold promise for future clinical applications. © 2007 Elsevier B.V. All rights reserved.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2007-01-01 | Brain research |