Abstract
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 language | English |
|---|---|
| Pages (from-to) | 911-920 |
| Number of pages | 10 |
| Journal | Journal of Leukocyte Biology |
| Volume | 91 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Jun 2012 |
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Keywords
- Adhesion molecules
- Apoptosis
- Circulatory shock
- Cytokines
- Fatty acid ethanolamide family
ASJC Scopus subject areas
- Cell Biology
- Immunology
Cite this
Effects of palmitoylethanolamide on intestinal injury and inflammation caused by ischemia-reperfusion in mice. / di Paola, Rosanna; Impellizzeri, Daniela; Torre, Agata; Mazzon, Emanuela; Cappellani, Alessandro; Faggio, Caterina; Esposito, Emanuela; Trischitta, Francesca; Cuzzocrea, Salvatore.
In: Journal of Leukocyte Biology, Vol. 91, No. 6, 06.2012, p. 911-920.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of palmitoylethanolamide on intestinal injury and inflammation caused by ischemia-reperfusion in mice
AU - di Paola, Rosanna
AU - Impellizzeri, Daniela
AU - Torre, Agata
AU - Mazzon, Emanuela
AU - Cappellani, Alessandro
AU - Faggio, Caterina
AU - Esposito, Emanuela
AU - Trischitta, Francesca
AU - Cuzzocrea, Salvatore
PY - 2012/6
Y1 - 2012/6
N2 - 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.
AB - 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.
KW - Adhesion molecules
KW - Apoptosis
KW - Circulatory shock
KW - Cytokines
KW - Fatty acid ethanolamide family
UR - http://www.scopus.com/inward/record.url?scp=84861933947&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84861933947&partnerID=8YFLogxK
U2 - 10.1189/jlb.0911485
DO - 10.1189/jlb.0911485
M3 - Article
C2 - 22469754
AN - SCOPUS:84861933947
VL - 91
SP - 911
EP - 920
JO - Journal of Leukocyte Biology
JF - Journal of Leukocyte Biology
SN - 0741-5400
IS - 6
ER -