Palmitoylethanolamide promotes anti-inflammatory phenotype of macrophages and attenuates plaque formation in ApoE-/- mice

Aim: The endogenous fatty acid amide palmitoylethanolamide (PEA) is a lipid-derived mediator, which does not bind to the cannabinoid receptors CB1 and CB2, but exerts potent anti-inflammatory effects by ligating type-α peroxisome proliferator-activated receptors (PPAR-α). PEA has shown to possess therapeutic potential in inflammatory disease models, but the role of PEA and its promise as a therapeutic agent in atherosclerosis remain unexplored. We aimed to evaluate the therapeutic potential of chronic PEA treatment in atherosclerotic mice.