Use este identificador para citar ou linkar para este item: http://hdl.handle.net/11690/3834
Autor(es): Cioato, Stefania Giotti
Medeiros, Liciane Fernandes
Lopes, Bettega Costa
Medeiros, Helouise Richardt
Caumo, Wolnei
Roesler, Rafael
Torres, Iraci L.S.
Título: A3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic pain
Palavras-chave: Adenosine A3 receptor;Cytokine;DMSO;IB-MECA;Neuropathic pain;Neurotrophin;Rats
Data do documento: 2022
Editor: CLINICAL AND BIOMEDICAL RESEARCH
Citação: CIOATO, S. G. et al. A3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic pain. CLINICAL AND BIOMEDICAL RESEARCH, v. 42, p. 128-134, 2022. Disponível em: https://seer.ufrgs.br/index.php/hcpa/article/view/116706/85500. Acesso em:22 fev.2024
Resumo: Introduction: Considering the lack of specific treatments for neuropathic pain, this study aimed to evaluate the effect of a single dose of adenosine A3 receptor IB-MECA on inflammatory and neurotrophic parameters in rats subjected to a neuropathic pain model. Methods: 64 adult male Wistar rats were used. Neuropathic pain was induced by chronic constriction injury (CCI) of the sciatic nerve and the treatment consisted of a 0.5 μmol/kg dose of IB-MECA, a selective A3 adenosine receptor agonist, dissolved in 3% DMSO; vehicle groups received DMSO 3% in saline solution, and morphine groups received 5 mg/kg. Cerebral cortex and hippocampus IL-1β, BDNF, and NGF levels were determined by Enzyme-Linked Immunosorbent assay. Results: The main outcome was that a single dose of IB-MECA was able to modulate the IL-1β hippocampal levels in neuropathic pain induced by CCI and the DMSO increased IL-1β and NGF hippocampal levels in sham-operated rats. However, we did not observe this effect when the DMSO was used as vehicle for IB-MECA, indicating that IB-MECA was able to prevent the effect of DMSO. Conclusions: Considering that the IL-1β role in neuropathic pain and the contributions of the hippocampus are well explored, our result corroborates the relationship between the A3 receptor and the process of chronic pain maintenance.
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