Modulation of synergism COX-1 with COX-2 in the tail flick of mice

Noriega Viviana 1, 2, Sierralta Fernando 3, Sotomayor-Zárate Ramón 4, Prieto Juan Carlos 2, 3 and Miranda Hugo F 5, *

1 Faculty of Medicine, Clínica Alemana, Universidad del Desarrollo, Chile.
2 Cardiovascular Department; Clinical Hospital, Universidad de Chile, Santiago, Chile.
3 Pharmacology Program, ICBM, Faculty of Medicine, Universidad de Chile, Santiago, Chile.
4 Laboratory of Neurochemistry and Neuropharmacology, Faculty of Sciences Universidad de Valparaíso, Valparaíso, Chile
5 Neuroscience Department, Faculty of Medicine, Universidad de Chile, Santiago, Chile.
 
Research Article
World Journal of Advanced Research and Reviews, 2020, 06(03), 222-228
Article DOI: 10.30574/wjarr.2020.6.3.0200
 
Publication history: 
Received on 11 June 2020; revised on 20 June 2020; accepted on 23 June 2020
 
Abstract: 
Nonsteroidal anti-inflammatory drugs (NSAIDs) are often used in the treatment of pain. In this study was evaluated, by isobolographic analysis, in a radiant heat model of mice, the tail flick, the potential antinociceptive pharmacological interaction of the combination between ketorolac and meloxicam and the modulation by tropisetron, risperidone, prazosin, yohimbine, naltrindole or 7-Nitroindazole. In the assay, the combination of ketorolac with meloxicam induces an additive interaction with an interaction index of 12.20 ± 0.92. Neither tropisetron nor risperidone nor prazosin nor yohimbine modify the nature of interaction, however naltrindole and 7-Nitroindazol change the nature of interaction from additive a subadditive with an interaction index of 16.85 ± 2.52 and 18.00 ± 2.57, respectively. The current results suggests that the interaction antinociceptive of the combination between ketorolac with meloxicam does not seem to be influenced by adrenergic, dopaminergic, histaminergic or serotonegic mechanisms. Nonetheless, the pretreatment of the mice with naltrindole or con 7-Nitroindazole induced a significant decrease in the antinociceptive power of the combination with a significant reduction in DE. It is suggested that DOR and NO may be involved, in the tail flick model, regulating the antinociceptive bioactivity of these NSAIDs.
 
Keywords: 
NSAIDs; Tail flick; Isobolographic analysis; Receptors antagonist
 
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