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Palmitoylethanolamide Reduces The Severity Of Brain Trauma In A Mouse Model Of Controlled Cortical Impact Injury
Author(s) -
Cuzzocrea Salvatore,
Ahmad Akbar,
Impellizzeri Daniela,
Mazzon Emanuela,
Esposito Emanuela
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.842.7
Subject(s) - medicine , palmitoylethanolamide , traumatic brain injury , neuroprotection , astrocyte , microglia , open field , rotarod performance test , edema , anesthesia , lesion , pathology , infiltration (hvac) , cerebral edema , inflammation , pharmacology , central nervous system , motor activity , physics , receptor , cannabinoid receptor , psychiatry , thermodynamics , agonist
After traumatic brain injury (TBI), the primary insult is followed by a cascade of secondary events which lead to enlargement of the primary lesion and are potentially amenable to therapeutic intervention. The goal of this study was to examine the acute effects of palmitoylethanolamide (PEA) on behavioral deficits, cerebral edema, mast cells (MCs) infiltration, and astrocyte/microglial activation in a murine model of TBI. Thirty male C57BL/6 mice underwent sham surgery, or cortical contusion impact injury (CCI). CCI mice received vehicle or PEA at 1 h after injury. Performance on the rotarod, forelimb cylinder, and open‐field tests were evaluated before and at 24 h after sham or CCI surgery. Cerebral edema was evaluated using the wet‐dry weight technique. Immunohistochemical analysis was used to examine changes in astrocyte/microglia‐specific protein immunoreactivity and mast cells infiltration. Locomotor performance and exploratory behavior were significantly improved in mice receiving PEA (10 mg/kg). Significant reductions were found for cerebral edema, iNOS and PAR immunoreactivity, MCs infiltration and number of activated glial cells in the injured brains from PEA‐treated mice. This study provides evidence of acute neuroprotective effects that may represent an avenue for further development of novel therapeutic agents in the treatment of TBI.

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