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https://repositorio.inpa.gov.br/handle/1/18483| Título: | Activation of peripheral κ/δ opioid receptors mediates 15-deoxy-Δ12,14-prostaglandin J2 induced-antinociception in rat temporomandibular joint |
| Autor: | Pena-Dos-Santos, Diego R. Severino, Fernando P. Lima Pereira, Sanívia Aparecida de Rodrigues, Denise Bertulucci Rocha Cunha, Fernando Queiroz Manfredo Vieira, Silvio Napimoga, Marcelo Henrique Napimoga, Juliana Trindade Clemente |
| Palavras-chave: | 15 Deoxy Delta12,14 Prostaglandin J2 1h 1,2,4 Oxadiazolo[4,3 A]quinoxalin 1 One 2 Chloro 5 Nitrobenzanilide Adenosine Triphosphate Sensitive Potassium Channel Aminoguanidine Arginine Delta Opiate Receptor Glibenclamide Guanylate Cyclase Kappa Opiate Receptor Naloxone Nitric Oxide Peroxisome Proliferator Activated Receptor Gamma Potassium Channel Blocking Agent 15 Deoxyprostaglandin J2 15 Deoxyprostaglandin J2 Adenosine Triphosphate Sensitive Potassium Channel Analgesic Agent Cyclic Gmp Delta Opiate Receptor Drug Derivative Formaldehyde Kappa Opiate Receptor Mu Opiate Receptor Nitric Oxide Synthase Peroxisome Proliferator Activated Receptor Gamma Prostaglandin D2 Serotonin Animals Cell Animals Experiment Animals Model Antiinflammatory Activity Antinociception Blood Vessel Permeability Cell Migration Controlled Study Drug Mechanism Inhibition Kinetics Male Neutrophil Nonhuman Pharmacological Blocking Priority Journal Rat Temporomandibular Joint Disorder Animals Chemically Induced Disorder Dose Response Drug Antagonism Drug Effect Inflammation Metabolism Pain Signal Transduction Temporomandibular Joint Wistar Rat Analgesics Animal Cyclic Gmp Dose-response Relationship, Drug Formaldehyde Inflammation Katp Channels Male Nitric Oxide Synthase Pain Ppar Gamma Prostaglandin D2 Rats Rats, Wistar Receptors, Opioid, Delta Receptors, Opioid, Kappa Receptors, Opioid, Mu Serotonin Signal Transduction Temporomandibular Joint |
| Data do documento: | 2009 |
| Revista: | Neuroscience |
| É parte de: | Volume 163, Número 4, Pags. 1211-1219 |
| Abstract: | This study assessed the effect of the agonist 15d- PGJ2 administered into the rat temporomandibular joint (TMJ) on nociceptive behavioral and the anti-inflammatory potential of this prostaglandin on TMJ. It was observed that 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) significantly reduced formalin-induced nociceptive behavior in a dose dependent manner, however injection of 15d-PGJ2 into the contralateral TMJ failed to reduce such effects. This antinociceptive effect is dependent on peroxisome proliferator-activated receptors-γ (PPAR-γ) since pre-treatment with GW9662 (PPAR-γ receptor antagonist) blocked the antinociceptive effect of 15d-PGJ2 in the TMJ. In addition, the antinociceptive effect of 15d-PGJ2 was also blocked by naloxone suggesting the involvement of peripheral opioids in the process. Confirming this hypothesis pre-treatment with κ, δ, but not μ receptor antagonists significantly reduced the antinociceptive effect of 15d-PGJ2 in the TMJ. Similarly to opioid agonists, the 15d-PGJ2 antinociceptive action depends on the nitric oxide (NO)/guanilate cyclase (cGMP)/ATP-sensitive potassium channel blocker(K+ATP) channel pathway since it was prevented by the pre-treatment with the inhibitors of nitric oxide synthase (NOS; aminoguanidine), cGMP (ODQ), or the K+ATP (glibenclamide). In addition, 15d-PGJ2 (100 ng/TMJ) inhibits 5-HT-induced TMJ hypernociception. Besides, TMJ treated with 15d-PGJ2 showed lower vascular permeability, assessed by Evan's Blue extravasation, and also lower neutrophil migration induced by carrageenan administration. Taken together, these results demonstrate that 15d-PGJ2 has a potential peripheral antinociceptive and anti-inflammatory effect in the TMJ via PPAR-γ activation. The results also suggest that 15d-PGJ2 induced-peripheral antinociceptive response in the TMJ is mediated by κ/δ opioid receptors by the activation of the intracellular L-arginine/NO/cGMP/K+ATP channel pathway. The pharmacological properties of the peripheral administration of 15d-PGJ2 highlight the potential use of this PPAR-γ agonist on TMJ inflammatory pain conditions. © 2009 IBRO. |
| DOI: | 10.1016/j.neuroscience.2009.07.052 |
| Aparece nas coleções: | Artigos |
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