期刊
SCIENTIFIC REPORTS
卷 7, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep44169
关键词
-
资金
- MRC Programme Grant [G1100356/1]
- MRC Career Development Award [MRC MR/M009238/1]
- BBSRC [BB/G002738/1] Funding Source: UKRI
- MRC [MR/M009238/1, G0901697, MR/P00265X/1, MR/N024524/1, G1100356] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/G002738/1] Funding Source: researchfish
- Medical Research Council [G1100356, MR/P00265X/1, MR/N024524/1, MR/M009238/1, G0901697] Funding Source: researchfish
- Wellbeing of Women [RG1436, RG1956] Funding Source: researchfish
Endometriosis is an incurable gynecological disorder characterized by debilitating pain and the establishment of innervated endometriosis lesions outside the uterus. In a preclinical mouse model of endometriosis we demonstrated overexpression of the PGE(2)-signaling pathway (including COX-2, EP2, EP4) in endometriosis lesions, dorsal root ganglia (DRG), spinal cord, thalamus and forebrain. TRPV1, a PGE(2)-regulated channel in nociceptive neurons was also increased in the DRG. These findings support the concept that an amplification process occurs along the pain neuroaxis in endometriosis. We then tested TRPV1, EP2, and EP4 receptor antagonists: The EP2 antagonist was the most efficient analgesic, reducing primary hyperalgesia by 80% and secondary hyperalgesia by 40%. In this study we demonstrate reversible peripheral and central hyperalgesia in mice with induced endometriosis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据