EP2 receptor antagonism reduces peripheral and central hyperalgesia in a preclinical mouse model of endometriosis.
作者： Erin Greaves , Andrew W. Horne , Helen Jerina , Marta Mikolajczak , Lisa Hilferty
DOI: 10.1038/SREP44169
关键词:
摘要: Endometriosis is an incurable gynecological disorder characterized by debilitating pain and the establishment of innervated endometriosis lesions outside uterus. In a preclinical mouse model we demonstrated overexpression PGE2-signaling pathway (including COX-2, EP2, EP4) in lesions, dorsal root ganglia (DRG), spinal cord, thalamus forebrain. TRPV1, PGE2-regulated channel nociceptive neurons was also increased DRG. These findings support concept that amplification process occurs along neuroaxis endometriosis. We then tested EP4 receptor antagonists: The EP2 antagonist most efficient analgesic, reducing primary hyperalgesia 80% secondary 40%. this study demonstrate reversible peripheral central mice with induced
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