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Campo DC | Valor | Idioma |
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dc.contributor.author | Pena-Dos-Santos, Diego R. | - |
dc.contributor.author | Severino, Fernando P. | - |
dc.contributor.author | Lima Pereira, Sanívia Aparecida de | - |
dc.contributor.author | Rodrigues, Denise Bertulucci Rocha | - |
dc.contributor.author | Cunha, Fernando Queiroz | - |
dc.contributor.author | Manfredo Vieira, Silvio | - |
dc.contributor.author | Napimoga, Marcelo Henrique | - |
dc.contributor.author | Napimoga, Juliana Trindade Clemente | - |
dc.date.accessioned | 2020-06-15T21:55:37Z | - |
dc.date.available | 2020-06-15T21:55:37Z | - |
dc.date.issued | 2009 | - |
dc.identifier.uri | https://repositorio.inpa.gov.br/handle/1/18483 | - |
dc.description.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. | en |
dc.language.iso | en | pt_BR |
dc.relation.ispartof | Volume 163, Número 4, Pags. 1211-1219 | pt_BR |
dc.rights | Restrito | * |
dc.subject | 15 Deoxy Delta12,14 Prostaglandin J2 | en |
dc.subject | 1h 1,2,4 Oxadiazolo[4,3 A]quinoxalin 1 One | en |
dc.subject | 2 Chloro 5 Nitrobenzanilide | en |
dc.subject | Adenosine Triphosphate Sensitive Potassium Channel | en |
dc.subject | Aminoguanidine | en |
dc.subject | Arginine | en |
dc.subject | Delta Opiate Receptor | en |
dc.subject | Glibenclamide | en |
dc.subject | Guanylate Cyclase | en |
dc.subject | Kappa Opiate Receptor | en |
dc.subject | Naloxone | en |
dc.subject | Nitric Oxide | en |
dc.subject | Peroxisome Proliferator Activated Receptor Gamma | en |
dc.subject | Potassium Channel Blocking Agent | en |
dc.subject | 15 Deoxyprostaglandin J2 | en |
dc.subject | 15 Deoxyprostaglandin J2 | en |
dc.subject | Adenosine Triphosphate Sensitive Potassium Channel | en |
dc.subject | Analgesic Agent | en |
dc.subject | Cyclic Gmp | en |
dc.subject | Delta Opiate Receptor | en |
dc.subject | Drug Derivative | en |
dc.subject | Formaldehyde | en |
dc.subject | Kappa Opiate Receptor | en |
dc.subject | Mu Opiate Receptor | en |
dc.subject | Nitric Oxide Synthase | en |
dc.subject | Peroxisome Proliferator Activated Receptor Gamma | en |
dc.subject | Prostaglandin D2 | en |
dc.subject | Serotonin | en |
dc.subject | Animals Cell | en |
dc.subject | Animals Experiment | en |
dc.subject | Animals Model | en |
dc.subject | Antiinflammatory Activity | en |
dc.subject | Antinociception | en |
dc.subject | Blood Vessel Permeability | en |
dc.subject | Cell Migration | en |
dc.subject | Controlled Study | en |
dc.subject | Drug Mechanism | en |
dc.subject | Inhibition Kinetics | en |
dc.subject | Male | en |
dc.subject | Neutrophil | en |
dc.subject | Nonhuman | en |
dc.subject | Pharmacological Blocking | en |
dc.subject | Priority Journal | en |
dc.subject | Rat | en |
dc.subject | Temporomandibular Joint Disorder | en |
dc.subject | Animals | en |
dc.subject | Chemically Induced Disorder | en |
dc.subject | Dose Response | en |
dc.subject | Drug Antagonism | en |
dc.subject | Drug Effect | en |
dc.subject | Inflammation | en |
dc.subject | Metabolism | en |
dc.subject | Pain | en |
dc.subject | Signal Transduction | en |
dc.subject | Temporomandibular Joint | en |
dc.subject | Wistar Rat | en |
dc.subject | Analgesics | en |
dc.subject | Animal | en |
dc.subject | Cyclic Gmp | en |
dc.subject | Dose-response Relationship, Drug | en |
dc.subject | Formaldehyde | en |
dc.subject | Inflammation | en |
dc.subject | Katp Channels | en |
dc.subject | Male | en |
dc.subject | Nitric Oxide Synthase | en |
dc.subject | Pain | en |
dc.subject | Ppar Gamma | en |
dc.subject | Prostaglandin D2 | en |
dc.subject | Rats | en |
dc.subject | Rats, Wistar | en |
dc.subject | Receptors, Opioid, Delta | en |
dc.subject | Receptors, Opioid, Kappa | en |
dc.subject | Receptors, Opioid, Mu | en |
dc.subject | Serotonin | en |
dc.subject | Signal Transduction | en |
dc.subject | Temporomandibular Joint | en |
dc.title | Activation of peripheral κ/δ opioid receptors mediates 15-deoxy-Δ12,14-prostaglandin J2 induced-antinociception in rat temporomandibular joint | en |
dc.type | Artigo | pt_BR |
dc.identifier.doi | 10.1016/j.neuroscience.2009.07.052 | - |
dc.publisher.journal | Neuroscience | pt_BR |
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