| First Author | Di Paola R | Year | 2012 |
| Journal | J Leukoc Biol | Volume | 91 |
| Issue | 6 | Pages | 911-20 |
| PubMed ID | 22469754 | Mgi Jnum | J:184907 |
| Mgi Id | MGI:5426726 | Doi | 10.1189/jlb.0911485 |
| Citation | Di Paola R, et al. (2012) Effects of palmitoylethanolamide on intestinal injury and inflammation caused by ischemia-reperfusion in mice. J Leukoc Biol 91(6):911-20 |
| abstractText | 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-alpha 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-alpha, IL-1beta), adhesion molecules (ICAM-1, P-selectin) expression, NF-kappaB 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-alpha, we have investigated the effect of PEA in PPAR-alpha 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-alpha 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. |
