Palmitoylethanolamide, a naturally-occurring lipid, is an orally effective intestinal anti-inflammatory agent. (Articolo in rivista)

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Label
  • Palmitoylethanolamide, a naturally-occurring lipid, is an orally effective intestinal anti-inflammatory agent. (Articolo in rivista) (literal)
Anno
  • 2014-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1111/bph.12907 (literal)
Alternative label
  • Borrelli F, Romano B, Petrosino S, Pagano E, Capasso R, Coppola D, Battista G, Orlando P, Di Marzo V, Izzo AA (2014)
    Palmitoylethanolamide, a naturally-occurring lipid, is an orally effective intestinal anti-inflammatory agent.
    in British journal of pharmacology
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Borrelli F, Romano B, Petrosino S, Pagano E, Capasso R, Coppola D, Battista G, Orlando P, Di Marzo V, Izzo AA (literal)
Rivista
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  • PubMe (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • ICB-CNR IBP-CNR Department of Pharmacy, University of Naples Federico II, via D Montesano 49, 80131 Naples, Italy Ospedale dei Pellegrini, Department of Diagnostic Services (Anatomy and Pathologic Histology Service), ASL 1, Naples, Italy (literal)
Titolo
  • Palmitoylethanolamide, a naturally-occurring lipid, is an orally effective intestinal anti-inflammatory agent. (literal)
Abstract
  • BACKGROUND AND PURPOSE Palmitoylethanolamide (PEA) acts via several targets, including cannabinoid CB1 and CB2 receptors, transient receptor potential vanilloid type-1 (TRPV1) ion channels, peroxisome proliferator-activated receptor alpha (PPAR ?) and orphan G protein-coupled receptor 55 (GRR55), all involved in the control of intestinal inflammation. Here, we investigated the effect of PEA in a murine model of colitis. EXPERIMENTAL APPROACH Colitis was induced in mice by intracolonic administration of dinitrobenzenesulfonic acid (DNBS). Inflammation was assessed by evaluating inflammatory markers/parameters and by histology; intestinal permeability by a fluorescent method; colonic cell proliferation by immunohistochemistry; PEA and endocannabinoid levels by liquid chromatography mass spectrometry; receptor and enzyme mRNA expression by quantitative RT-PCR. KEY RESULTS DNBS administration caused inflammatory damage, increased colonic levels of PEA and endocannabinoids, down-regulation of mRNA for TRPV1 and GPR55 but no changes in mRNA for CB1, CB2 and PPAR?. Exogenous PEA (i.p. and/or p.o., 1 mg·kg-1) attenuated inflammation and intestinal permeability, stimulated colonic cell proliferation, and increased colonic TRPV1 and CB1 receptor expression. The anti-inflammatory effect of PEA was attenuated or abolished by CB2 receptor, GPR55 or PPAR? antagonists and further increased by the TRPV1 antagonist capsazepine. CONCLUSIONS AND IMPLICATIONS PEA improves murine experimental colitis, the effect being mediated by CB2 receptors, GPR55 and PPAR?, and modulated by TRPV1 channels. Abbreviations 2-AG, 2-arachidonoylglycerol; CB, cannabinoid; DNBS, 2,4,6-dinitrobenzenesulfonic acid; DSS, dextran sodium sulphate; FAAH, fatty acid amide hydrolase; GDE1, glycerophosphodiester PDE 1; IBD, inflammatory bowel disease; MPO, myeloperoxidase; NAAA, N-acylethanolamine-hydrolysing acid amidase; NAPE-PLD, N-arachidonyl-phosphatidylethanolamine PLD; OEA, oleoylethanolamide; PEA, palmitoylethanolamide; TRPV1, transient receptor potential vanilloid type-1 (literal)
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