At the EFIC pain congress in Florence, 2013 a paper on the mechanism of action of palmitoylethanolamide was presented by Dr. S. Assaw from the School of Biomedical Sciences, University of Nottingham, Nottingham, UK.
In the rat model PEA significantly reduced carrageenan-induced pain behaviour 2 hours post-injection, and significantly reduced recruitment of monocytic cells whereas neutrophil numbers were unaltered. Gene expression analysis indicated differential effects of PEA on expression of pro-inflammatory and other genes involved in innate immune response. The conclusion of the presentation was:
The differential effect of PEA on immune cell recruitment and gene expression
indicates an effect on specific pathways rather than a general anti-inflammatory effect of PEA in the carrageenan model. This may suggest that the analgesic effects of the nuclear receptor PPAR-α arise from a targeted regulation of specific components of the inflammatory signalling process.