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The role of endogenous opioid peptides in the antinociceptive effect of 15-deoxyΔ12,14-prostaglandin J2 in the temporomandibular joint
被引:12
作者:
Macedo, C. G.
[1
]
Napimoga, M. H.
[2
]
Rocha-Neto, L. M.
[1
]
Abdalla, H. B.
[1
]
Clemente-Napimoga, J. T.
[1
]
机构:
[1] Univ Campinas UNICAMP, Piracicaba Dent Sch, Dept Physiol Sci, Lab Orofacial Pain, Av Limeira 901, BR-13414903 Piracicaba, SP, Brazil
[2] Rio Leopoldo Mand Inst & Res Ctr, Lab Immunol & Mol Biol, Rua Jose Rocha Junqueira 13, BR-13045755 Campinas, SP, Brazil
来源:
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
|
2016年
/
110卷
基金:
巴西圣保罗研究基金会;
关键词:
ACTIVATED-RECEPTOR-GAMMA;
TRANSIENT FOCAL ISCHEMIA;
SPINAL-CORD-INJURY;
15-DEOXY-DELTA(12,14)-PROSTAGLANDIN J(2);
INFLAMMATORY PAIN;
NEUROPATHIC PAIN;
PERIPHERAL ANTINOCICEPTION;
NEUTROPHIL MIGRATION;
SIGNALING PATHWAY;
RATS;
D O I:
10.1016/j.plefa.2016.05.009
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
We have previously demonstrated that peripheral administration of 15d-PGJ(2) in the Temporomandibular joint (TMJ) of rats can prevent nociceptor sensitization, mediated by peroxisome proliferator activated receptor-gamma (PPAR-gamma), and kappa- and delta- opioid receptors. However, the mechanism that underlies the signaling of PPAR-gamma (upon activation by 15d-PGJ(2)) to induce antinociception, and how the opioid receptors are activated via 15d-PGJ(2) are not fully understood. This study demonstrates that peripheral antinociceptive effect of 15d-PGJ(2) is mediated by PPAR-gamma expressed in the inflammatory cells of TMJ tissues. Once activated by 15d-PGJ(2), PPAR-gamma induces the release of beta-endorphin and dynorphin, which activates kappa- and delta-opioid receptors in primary sensory neurons to induce the antinociceptive effect. (C) 2016 Elsevier Ltd. All rights reserved.
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页码:27 / 34
页数:8
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