Does COX2-dependent PGE2 play a role in neuropathic pain?
作者： Weiya Ma , Rémi Quirion
DOI: 10.1016/J.NEULET.2008.02.072
关键词:
摘要: Neuropathic pain (NeP) is a common chronic state with unmet medical needs. Due to poorly defined underlying mechanisms, current therapies for NeP are far from satisfactory. Mounting evidence suggests that long-term plasticity in signaling pathways underpins the pathogenesis of NeP. Inflammatory responses injured nerves have been recognized as important events initially sensitizing nociceptive neurons and subsequently inducing dorsal root ganglion. cells such invading macrophages Schwann produce wide array inflammatory mediators. Cyclooxygenase 2-dependent prostaglandin E2 (COX2/PGE2) one mediator abundantly produced involved genesis In this mini-review, we highlight possible novel mechanisms role COX2/PGE2 Long lasting may induce effects on nociceptors facilitate synthesis pain-related molecules by stimulating 'en passant' or spared axons. also local mediators via autocrine paracrine pathways. downstream PGE2 EP receptor should be considered therapeutic targets more effectively treat
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