Role of PPAR-α, PPAR-γ, and PPAR-δ in palmitoylethanolamide-induced inhibition of inducible nitric oxide synthase expression. Spinal cord injury (SCI) induced an increase in inducible nitric oxide synthase (iNOS) expression evaluated by western blot analysis. Palmitoylethanolamide (PEA) post-treatment significantly reduced the levels of this protein in spinal cord homogenates. Either pretreatment with GW9662 (1 mg/kg) or GSK0660 (1mg/kg) counteracted the anti-inflammatory action of PEA (A). Mice with genetic absence of the peroxisome proliferator-activated receptor (PPAR)-α receptor exhibited increased expression of iNOS when compared with that observed in the SCI wildtype (WT) group and PEA was not able to reduce the expression of this enzyme in injured PPAR-αKO mice (B). *P <0.05 vs. sham WT; **P <0.01 vs. sham WT group; ##P <0.01 vs. SCI WT group.