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Effects of palmitoylethanolamide on signaling pathways implicated in the development of spinal cord injury.

Abstract
Activation of peroxisome proliferator-activated receptor (PPAR)-alpha, a member of the nuclear receptor superfamily, modulates inflammation and tissue injury events associated with spinal cord trauma in mice. Palmitoylethanolamide (PEA), the naturally occurring amide of palmitic acid and ethanolamine, reduces pain and inflammation through a mechanism dependent on PPAR-alpha activation. The aim of the present study was to evaluate the effect of the PEA on secondary damage induced by experimental spinal cord injury (SCI) in mice. SCI was induced by application of vascular clips to the dura mater via a four-level T(5)-T(8) laminectomy. This resulted in severe trauma characterized by edema, neutrophil infiltration, and production of inflammatory mediators, tissue damage, and apoptosis. Repeated PEA administration (10 mg/kg i.p.; 30 min before and 1 and 6 h after SCI) significantly reduced: 1) the degree of spinal cord inflammation and tissue injury, 2) neutrophil infiltration, 3) nitrotyrosine formation, 4) proinflammatory cytokine expression, 5) nuclear transcription factor activation-kappaB activation, 6) inducible nitric-oxide synthase expression, and 6) apoptosis. Moreover, PEA treatment significantly ameliorated the recovery of motor limb function. Together, the results indicate that PEA reduces inflammation and tissue injury associated with SCI and suggest a regulatory role for endogenous PPAR-alpha signaling in the inflammatory response associated with spinal cord trauma.
AuthorsTiziana Genovese, Emanuela Esposito, Emanuela Mazzon, Rosanna Di Paola, Rosaria Meli, Placido Bramanti, Daniele Piomelli, Antonio Calignano, Salvatore Cuzzocrea
JournalThe Journal of pharmacology and experimental therapeutics (J Pharmacol Exp Ther) Vol. 326 Issue 1 Pg. 12-23 (Jul 2008) ISSN: 1521-0103 [Electronic] United States
PMID18367664 (Publication Type: Comparative Study, Journal Article)
Chemical References
  • Amides
  • Endocannabinoids
  • Ethanolamines
  • Palmitic Acids
  • palmidrol
  • Nitric Oxide Synthase Type II
Topics
  • Amides
  • Animals
  • Endocannabinoids
  • Ethanolamines
  • Male
  • Mice
  • Motor Skills (drug effects, physiology)
  • Nitric Oxide Synthase Type II (biosynthesis, genetics)
  • Palmitic Acids (pharmacology, therapeutic use)
  • Recovery of Function
  • Signal Transduction (drug effects, physiology)
  • Spinal Cord Injuries (drug therapy, metabolism, pathology)
  • Thoracic Vertebrae (drug effects, metabolism, pathology)

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