Background Non-steroidal anti-inflammatory drugs (NSAIDs) may act through others mechanisms, in addition to inhibition of prostaglandin synthesis. These includes cholinergic, NO, serotonergic and opioids pathways. Methods The aim of this work was to evaluate the effect of systemic action of (S)-+-ketoprofen (dexketoprofen, DEX) on pain behaviors using the orofacial formalin test in mice and the potential involvement of cholinergic, NO, serotonergic and opioids pathways. Results The pretreatment of the mice with 1 mg/kg ip of atropine or opoid antagonists: 1 mg/kg, ip of NTX or 1 mg/kg ip of NTI or 1 mg/kg of NOR-BNI ip, did not produce significant change in the ED50 values of the antinociception to orofacial test induced by DEX. The pretreatment of the mice with 0.5 mg/kg ip tropisetron, increased in a significant fashion the values of ED50 of DEX. When the mice were treated with 5 mg/kg ip of L-NAME or 25 mg/kg ip of aminoguanidine or 50 mg/kg ip of 7-nitroindazole reversed the antinociception of DEX. Conclusion The findings of this study demonstrate activation of NO and 5-HTpathways play important roles in the systemic antinociceptive effect of DEX in a murine model of inflammatory pain.
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