• Jôice D Correa, Patrícia Paiva-Lima, Rafael M Rezende, Webster G P Dos Reis, Dalton L Ferreira-Alves, Y S Bakhle, and Janetti N Francischi.
• Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
• Life Sci. 2010 Jun 19;86(25-26):951-6.

AimsThe endogenous opioids mediate the analgesic effects of celecoxib in a model of mechanical hyperalgesia in rats. As responses to thermal stimuli may differ from those to mechanical stimuli, we have here assessed celecoxib in a rat model of thermal hyperalgesia and the possible involvement of endogenous opioids and their corresponding receptors in these effects.Main MethodsInjection of carrageenan (CG) into one hind paw induced a dose-related hyperalgesia (decreased time for paw withdrawal) to thermal stimuli (infra-red light beam), over 6h.Key FindingsCelecoxib (sc) 30 min before CG (250 microg per paw) induced a dose-dependent reversal of hyperalgesia, with withdrawal times well above basal levels, characterizing development of hypoalgesia. Indomethacin (sc) reversed CG-induced hyperalgesia only to basal levels (an anti-hyperalgesic effect). Naltrexone (sc) prevented hypoalgesia after celecoxib but did not change the response to indomethacin. Local (intraplantar) injection of either a selective antagonist of mu-(beta-funaltrexamine), kappa-(nor-binaltorphimine) or of delta-(naltrindole) opioid receptors also reversed the hypoalgesic effects of celecoxib, without modifying the hyperalgesia due to CG or affecting the nociceptive thresholds in the non-injected paw.SignificanceOur data show that celecoxib, unlike indomethacin, was hypoalgesic in this model of thermal hyperalgesia, and that this effect was mediated by peripheral mu-, kappa- and delta-opioid receptors.Copyright 2010 Elsevier Inc. All rights reserved.

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