The contrasting pro-inflammatory and pro-nociceptive roles of bioactive lipid mediators are well established [36, 37]. The COX branch of the AA cascade leads to prostanoids which generate pain directly in addition to sensitizing nociceptors [38]. The LOX branch leads to leukotrienes which are thought mostly to sensitize nociceptors via transient receptor potential vanilloid type I channels (TRPV1) [39]. The anti-inflammatory and anti-nociceptive effects of the EETs, products of the cytochrome P450, however were unexpected because the AA cascade is overall viewed as a major inflammatory pathway which increases nociception.
