Affiliations: [a] Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, USA | [b] Medical University of Lublin, Lublin, Poland | [c] Neuroscience Research, R&D, Jesse Brown VA Medical Center, Chicago, IL, USA | [d] Department of Pediatrics, University of Illinois at Chicago, Chicago, IL, USA
Correspondence:
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Corresponding author: Neelima B. Chauhan, PhD, R&D (151), Jesse Brown VA Medical Center; 820 South Damen Avenue, Chicago, IL 60612-3728, USA. Tel.: +1 312 569 7747; Fax: +1 312 569 8114; E-mail: [email protected]
Abstract: Purpose:Traumatic brain injury (TBI) is one of the leading causes of disability and death which begins with the formation of edema as the persistent primary causative factor in TBI. Although medical management of cerebral edema by hypothermia, ventriculostomy, mannitol or hypertonic saline have been effective in treating edema, many of these therapies end up with some neurologic deficits, necessitating novel treatment options for treating post-TBI edema. This study investigated edema reducing effects of recombinant human Erythropoietin (rhEPO) in reducing acute brain edema in the CCI mouse model of TBI. Methods:Anti-edema effects of rhEpo in reducing acute brain edema after injury in the CCI mouse model of TBI were assessed by T2 weighted magnetic resonance imaging (T2wMRI) as the accurate detector of brain edema in correlation with Western blot analysis of cerebral aquaporin 4 (AQP4) index as the critical marker of edema. Results:Results show that rhEpo treatment significantly reduced brain edema with concomitant reduction in AQP4 immunoexpression in the CCI mouse model of TBI. Conclusion:Current results emphasize clinical utility of rhEpo in treating post-TBI edema.
Keywords: Traumatic brain injury, controlled cortical impact injury, recombinant human erythropoietin, magnetic resonance imaging, edema, AQP4
