Avaliação do envolvimento do receptor FPR2/ALXR periférico e espinal no efeito anti-hiperalgésico induzido pela eletroacupuntura

Detalhes bibliográficos
Ano de defesa: 2018
Autor(a) principal: Caron, Cintia Vieira
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Não Informado pela instituição
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: https://repositorio.animaeducacao.com.br/handle/ANIMA/3052
Resumo: Although the effects of electroacupuncture (EA) on pain and inflammation are similar to the activation effects of formyl peptide receptor 2 (FPR2/ALXR) mediated by pro-resolving substances, the involvement of this receptor in the antihyperalgesic effect of EA had not yet been investigated. Objective: To evaluate the involvement of the peripheral and spinal FPR2/ALXR receptor in the antihyperalgesic effect induced by low-frequency EA in an animal model of persistent peripheral inflammation. Methods: Swiss male mice (30 to 40 g) underwent intraplantar (i.pl.) injection with complete Freund's adjuvant (CFA). Mechanical hyperalgesia was assessed by the von Frey test. The animals were treated with EA (in SP6 and ST36 acupoints) or BML-111 (an analog of lipoxin A4 [LXA4]) for 5 consecutive days. In the analysis of the mechanism of action the mice were treated on the first and fifth day. The edema was evaluated on the fourth day after CFA by measuring the thickness of the paw. Intraplantar (i.pl.) and intrathecal (i.t.) administration of the FPR2/ALXR receptor antagonist (WRW4) or naloxone were performed on the first and fifth day after CFA. Expression of the FPR2/ALXR receptor in the paw and spinal cord was performed on the second day after CFA by the Western Blotting technique. Results: EA and BML-111 reduced mechanical hyperalgesia. Daily treatment for 4 consecutive days with EA or BML-111 did not reduce paw edema. The i.pl. or i.t. pre-treatment of animals with WRW4 or naloxone prevented the antihyperalgesic effect induced by EA or BML-111. The CFA i.pl. injection increased FPR2/ALXR receptor expression in the paw, but not in the spinal cord. Treatment of animals with EA or BML-111 did not alter FPR2/ALXR receptor expression in the paw or spinal cord, although animals treated with EA or BML-111 when pretreated with WRW4 had lower FPR2/ALXR receptor expression in the spinal cord. However, lower expression of the FPR2/ALXR receptor in the paw was evidenced only in animals pretreated with WRW4 that received EA treatment. Conclusion: Treatment with EA or BML-111 reduced mechanical hyperalgesia, but not edema, and this effect might be mediated by activation of peripheral and central FPR2/ALXR receptor.