[22]. In support of this hypothesis of central action we demonstrated that inhibition of sEH significantly suppressed the up-regulation of spinal COX-2 mRNA. This effect is of course expected from an anti-inflammatory agent that penetrates into the CNS and prevents nuclear translocation of NFκB. Thus suppression of COX-2 expression contributes significantly to the anti-nociceptive properties of sEHIs, at least in models of inflammatory pain.
