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Figure 3 | Journal of Neuroinflammation

Figure 3

From: Molecular evidence for the involvement of PPAR-δ and PPAR-γ in anti-inflammatory and neuroprotective activities of palmitoylethanolamide after spinal cord trauma

Figure 3

Role of peroxisome proliferator-activated receptors in palmitoylethanolamide-induced TNFα and IL-1β inhibition after spinal cord trauma. Wildtype (WT) mice showed a significant production of cytokines 24 hours after spinal cord compression (A), (B). Cytokine levels were enhanced in peroxisome proliferator-activated receptor (PPAR)-αKO mice when compared with the spinal cord injury (SCI) WT group. Treatment with palmitoylethanolamide (PEA, 10 mg/kg) significantly reduced the spinal cord TNFα (A) and IL-1β (B) production. The genetic absence of the PPAR-α receptor, as well as GSK0660 or GW9662 pretreatment, significantly blocked this reduction. Data are mean ± standard error of the mean of 10 mice for each group. *P <0.05 vs. sham WT; **P <0.01 vs. sham WT group; #P <0.05 vs. SCI WT group.

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