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Palmitoylethanolamide reduces inflammation and itch in a mouse model of contact allergic dermatitis.pdf
European Journal of Pharmacology 791 (2016) 669–674
Contents lists available at ScienceDirect
European Journal of Pharmacology
journal homepage: /locate/ejphar
Immunopharmacology and in?ammation
crossmarkPalmitoylethanolamide reduces in?ammation and itch in a mouse model of
contact allergic dermatitis
Massimo Vaiaa, Stefania Petrosinob,c,d, Daniele De Filippisa, Luana Negroa, Andrea Guarinoa, Rosa Carnuccioa, Vincenzo Di Marzob,c,?, Teresa Iuvonea,c,?
a Department of Pharmacy, University of Naples Federico II, Via D. Montesano 49, 80131 Napoli, Italy b Istituto di Chimica Biomolecolare (ICB), Consiglio Nazionale delle Ricerche, Via Campi Flegrei 34, 80078 Pozzuoli, NA, Italy c Endocannabinoid Research Group, Italy d Epitech Group S.p.A., Via Luigi Einaudi 13, 35030 Saccolongo, PD, Italy
ARTICLE INFO
Keywords: Angiogenesis Contact allergic dermatitis (CAD) Dinitro?uorobenzene (DNFB) Itch Mast cells (MCs) Palmitoylethanolamide (PEA)
ABSTRACT
In mice, 2,4-dinitro?uorobenzene (DNFB) induces contact allergic dermatitis (CAD), which, in a late phase, is characterized by mast cell (MC) in?ltration and angiogenesis. Palmitoylethanolamide (PEA), an endogenous anti-in?ammatory molecule, acts by down-modulating MCs following activation of the cannabinoid CB2 receptor and peroxisome proliferator-activated receptor-α (PPAR-α). We have previously reported the antiin?ammatory e?ect of PEA in the early stage of CAD. Here, we examined whether PEA reduces the features of the late stage of CAD including MC activation, angiogenesis and itching. After sensitization to DNFB, female C57BL/6J mice underwent to three DNFB challenges at days 5, 12 and 19 and treatments were given at each challenge and for two more days. CAD was expressed as Δ increase in ear thickness between challenged and unchallenged mice. PEA (5 mg/kg/i.p.) reduced: i) the DNFB-induced Δ increase; ii) the number of MCs per tissue area; iii) the expression of VEGF and its receptor Flk-1. These e?ects were reversed by co-a
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