Journal
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
Volume 105, Issue -, Pages 157-165Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pbb.2013.02.006
Keywords
Nitric oxide donor; [Ru(bpy)(2)(NO)SO3](EF6); Guanylate cyclase; Protein kinase G; ATP sensitive K channels; Hyperalgesia; TRPV1; Capsaicin
Funding
- Fundacao Araucaria
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico [CNPq]
- Departamento de Ciencia e Tecnologia da Secretaria de Ciencia, Tecnologia e Insumos Estrategicos
- Ministerio da Saude (Decit/SCTIE/MS)
- Fundacao Araucaria/SETI-PR, Parana State Government
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
- CNPq
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The activation of nitric oxide (NO) production is an analgesic mechanism shared by drugs such as morphine and diclofenac. Therefore, the controlled release of low amounts of NO seems to be a promising analgesic approach. In the present study, the antinociceptive effect of the ruthenium NO donor [Ru(bpy)(2)(NO)SO3](PF6) (complex I) was investigated. It was observed that complex I inhibited in a dose (0.3-10 mg/kg)-dependent manner the acetic acid-induced writhing response. At the dose of 1 mg/kg, complex I inhibited the phenyl-p-benzoquinone-induced writhing response and formalin- and complete Freund's adjuvant-induced licking and flinch responses. Additionally, complex I also inhibited transient receptor potential cation channel subfamily V member 1 (TRPV1)-dependent overt pain-like behavior induced by capsaicin. Complex I also inhibited the carrageenin-induced mechanical hyperalgesia and increase of myeloperoxidase activity (MPO) in paw skin samples. The inhibitory effect of complex I in the carrageenin-induced hyperalgesia, MPO activity and formalin was prevented by the treatment with ODQ KT5823 and glybenclamide, indicating that complex I inhibits inflammatory hyperalgesia by activating the cGMP/PKG/ATP-sensitive potassium channel signaling pathway. The present study demonstrates the efficacy of a novel ruthenium NO donor and its analgesic mechanisms. (C) 2013 Elsevier Inc. All rights reserved.
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