Please use this identifier to cite or link to this item: http://hdl.handle.net/11690/1907
Authors: Cioato, Stefania Giotti
Medeiros, Liciane Fernandes
Lopes, Bettega Costa
Souza, Andressa de
Medeiros, Helouise Richardt
Assumpção, José Antônio Fagundes
Caumo, Wolnei
Roesler, Rafael
Torres, Iraci L. S.
Title: Antinociceptive and neurochemical effects of a single dose of IB-MECA in chronic pain rat models
Keywords: Adenosine receptor;Biomarkers;Inflammatory pain;Neuropathic pain;Rats
Issue Date: 2020
Publisher: Springer
Citation: CIOATO, S. G. et al. Antinociceptive and neurochemical effects of a single dose of IB-MECA in chronic pain rat models. Purinergic Signalling, v. 16, n. 4, p. 576-584, dez., 2020. Disponível em: https://link.springer.com/article/10.1007%2Fs11302-020-09751-w. Acesso em: 02 ago. 2021.
Abstract: This study aimed to evaluate the effect of a single administration of IB-MECA, an A3 adenosine receptor agonist, upon the nociceptive response and central biomarkers of rats submitted to chronic pain models. A total of 136 adult male Wistar rats were divided into two protocols: (1) chronic inflammatory pain (CIP) using complete Freund's adjuvant and (2) neuropathic pain (NP) by chronic constriction injury of the sciatic nerve. Thermal and mechanical hyperalgesia was measured using von Frey (VF), Randal-Selitto (RS), and hot plate (HP) tests. Rats were treated with a single dose of IB-MECA (0.5 μmol/kg i.p.), a vehicle (dimethyl sulfoxide-DMSO), or positive control (morphine, 5 mg/kg i.p.). Interleukin 1β (IL-1β), brain-derived neurotrophic factor (BDNF), and nerve growth factor (NGF) levels were measured in the brainstem and spinal cord using enzyme-linked immunosorbent assay (ELISA). The establishment of the chronic pain (CIP or NP) model was observed 14 days after induction by a decreased nociceptive threshold in all three tests (GEE, P < 0.05). The antinociceptive effect of a single dose of IB-MECA was observed in both chronic pain models, but this was more effective in NP model. There was an increase in IL-1β levels promoted by CIP. NP model promoted increase in the brainstem BDNF levels, which was reversed by IB-MECA.
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