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.

引用

页码：27 / 34

页数：8

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