Document Detail


Central cyclooxygenase inhibitors reduced IL-1beta-induced hyperalgesia in temporomandibular joint of freely moving rats.
MedLine Citation:
PMID:  16098663     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Microinjection of formalin (5%, 50 microl) into a temporomandibular joint (TMJ) causes noxious behavioral responses in freely moving rats. In the present study, we investigated the role of central cyclooxygenase (COX) pathways in IL-1beta-induced hyperalgesia with formalin-induced TMJ pain model. Intra-articular injection of 100 pg or 1 ng of IL-1beta significantly facilitated formalin-induced behavior by 130 or 174% in the number of scratches. Intracisternal administration of 100 pg or 1 ng of IL-1beta also significantly increased formalin-induced behavior by 166 or 82% in the number of scratches. IL-1beta-induced hyperalgesia was blocked by pretreatment with IL-1 receptor antagonist. Intracisternal pretreatment with SC-560, a selective COX-1 inhibitor, or NS-398, a selective COX-2 inhibitor, abolished intra-articular administration of IL-1beta-induced hyperalgesic response. Intracisternal pretreatment with NS-398, a selective COX-2 inhibitor, abolished the intracisternal administration of IL-1beta-induced hyperalgesic response, while pretreatment with SC-560, a selective COX-1 inhibitor, did not change IL-1beta-induced hyperalgesic responses. On the other hand, pretreatment with acetaminophen, a tentative COX-3 inhibitor, also abolished both intra-articular and intracisternal administration of IL-1beta-induced hyperalgesic responses. These results indicate that central COX-2 plays important role in the central administration of IL-1beta-induced hyperalgesia and that central COX-1/2 pathways mediate peripheral administration of IL-1beta-induced hyperalgesia in the TMJ. Central COX-3 inhibitor seems to play an important role in the nociceptive process associated with both peripheral and central administration of IL-1beta-induced hyperalgesia in TMJ. It is concluded that central acting of COX-3 inhibitors may be of therapeutic value in the treatment of inflammatory pain in TMJ.
Authors:
Dong K Ahn; Jong M Chae; Hyo S Choi; Hee M Kyung; Oh W Kwon; Hyo S Park; Dong H Youn; Yong C Bae
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Pain     Volume:  117     ISSN:  0304-3959     ISO Abbreviation:  Pain     Publication Date:  2005 Sep 
Date Detail:
Created Date:  2005-09-05     Completed Date:  2006-01-05     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7508686     Medline TA:  Pain     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  204-13     Citation Subset:  IM    
Affiliation:
Department of Oral Physiology, School of Dentistry, Kyungpook National University, 188-1 Sam Deok 2 ga, Chung-gu, Daegu 700-412, South Korea. dkahn@knu.ac.kr
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MeSH Terms
Descriptor/Qualifier:
Animals
Behavior, Animal / drug effects
Cyclooxygenase Inhibitors / administration & dosage*
Disease Models, Animal
Dose-Response Relationship, Drug
Drug Administration Routes
Drug Interactions
Evans Blue / diagnostic use
Formaldehyde
Hyperalgesia / chemically induced,  drug therapy*
Interleukin-1*
Male
Nitrobenzenes / administration & dosage*
Pyrazoles / administration & dosage*
Rats
Rats, Sprague-Dawley
Sulfonamides / administration & dosage*
Temporomandibular Joint Disorders / chemically induced,  physiopathology*
Time Factors
Wakefulness
Chemical
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Interleukin-1; 0/Nitrobenzenes; 0/Pyrazoles; 0/SC 560; 0/Sulfonamides; 123653-11-2/N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; 314-13-6/Evans Blue; 50-00-0/Formaldehyde

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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