Effects of palmitoylethanolamide on intestinal injury and inflammation caused by ischemia-reperfusion in mice

Rosanna di Paola, Daniela Impellizzeri, Agata Torre, Emanuela Mazzon, Alessandro Cappellani, Caterina Faggio, Emanuela Esposito, Francesca Trischitta, Salvatore Cuzzocrea

Research output: Contribution to journalArticlepeer-review


Our primary aim in this study was to test the hypothesis that PEA, a member of the fatty acid ethanolamide family and an endogenous PPAR-α ligand, exerts anti-inflammatory effects on SAO shock, causing a severe form of circulatory shock and enhanced formation of ROS. SAO shock was induced by clamping the superior mesenteric artery and the celiac trunk, resulting in a total occlusion of these arteries for 30 min. After this period of occlusion, the clamps were removed. In this study, we demonstrated that the administration of PEA, 5 min before reperfusion, significantly reduced all of the parameters involved during inflammation, such as proinflammatory cytokine production (TNF-α, IL-1β), adhesion molecules (ICAM-1, P-selectin) expression, NF-κB expression, and apoptosis (Bax, Bcl-2, TUNEL assay) activation. In addition, to study whether the protective action of PEA on SAO shock is also related to the activation of PPAR-α, we have investigated the effect of PEA in PPAR-α KO mice subjected to SAO shock. Our study clearly demonstrates that PEA significantly attenuated the degree of intestinal injury and inflammation caused by I/R injury. Moreover, the positive effects of PEA were at least in part dependent on the PPAR-α pathway. The results clearly indicate that PEA exerts an anti-inflammatory effect, also in a SAO shock model, which could imply a future use of PEA in the treatment of I/R shock.

Original languageEnglish
Pages (from-to)911-920
Number of pages10
JournalJournal of Leukocyte Biology
Issue number6
Publication statusPublished - Jun 2012


  • Adhesion molecules
  • Apoptosis
  • Circulatory shock
  • Cytokines
  • Fatty acid ethanolamide family

ASJC Scopus subject areas

  • Cell Biology
  • Immunology


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