COX-2 contributed to the remifentanil-induced hyperalgesia related to ephrinB/EphB signaling

ABSTRACTBackground and Objectives： Studying the underlying mechanisms of opiate-induced hyperalgesia is fundamental to understanding and treating pain. Our previous study has proved that ephrinB/EphB signaling contributes to opiate-induced hyperagesia, but the manner in which ephrinB/EphB signaling acts on spinal nociceptive information networks to produce hyperalgesia remains unclear. Other studies have suggested that ephrinB/EphB signaling, NMDA receptor and COX-2 act together to participate in the modulation of nociceptive information processes at the spinal level. The objective of this research was to investigate the role of COX-2 in remifentanil-induced hyperalgesia and its relationship with ephrinB/EphB signaling.Methods： We characterized the remifentanil-induced pain behaviours by evaluating thermal hyperalgesia and mechanical allodynia in a mouse hind paw incisional model. Protein expression of COX-2 in spinal cord was assayed by western blotting and mRNA level of COX-2 was assayed by Real-time PC...