• Eur. J. Pharmacol. · Apr 2021

    TNF-α, CXCL-1 and IL-1 β as activators of the opioid system involved in peripheral analgesic control in mice.

    • Jayane Laís Dias Quintão, Amanda Cristina Reis Gonzaga, Giovane Galdino, Lima RomeroThiago RobertoTRDepartment of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais (UFMG), Av. Antônio Carlos, 6627, 31.270-100, Belo Horizonte, Brazil., JosianeFernandes Silva, VirgíniaSoares Lemos, Gabriel Henrique Campolina-Silva, Cleida Aparecida de Oliveira, GermánArturo Bohórquez Mahecha, and IgorDimitri Gama Duarte.
    • Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais (UFMG), Av. Antônio Carlos, 6627, 31.270-100, Belo Horizonte, Brazil.
    • Eur. J. Pharmacol. 2021 Apr 5; 896: 173900.

    AbstractTissue injury results in the release of inflammatory mediators, including a cascade of nociceptive substances, which contribute to development of hyperalgesia. In addition, during this process endogenous analgesic substances are also peripherally released with the aim of controlling the hyperalgesia. Thus, the present study aimed to investigate whether inflammatory mediators TNF-α, IL-1β, CXCL1, norepinephrine (NE) and prostaglandin E2 (PGE2) may be involved in the deflagration of peripheral endogenous modulation of inflammatory pain by activation of the opioid system. Thus, male Swiss mice and the paw withdrawal test were used. All substances were injected by the intraplantar route. Carrageenan, TNF-α, CXCL-1, IL1-β, NE and PGE2 induced hyperalgesia. Selectives μ (clocinamox), δ (naltrindole) and κ (norbinaltorphimine, nor-BNI) and non-selective (naloxone) opioid receptor antagonists potentiated the hyperalgesia induced by carrageenan, TNF-α, CXCL-1 and IL1-β. In contrast, when the enzyme N-aminopeptidase involved in the degradation of endogenous opioid peptides was inhibited by bestatin, the hyperalgesia was significantly reduced. In addition, the western blotting assay indicated that the expression of the opioid δ receptor was increased after intraplantar injection of carrageenan. The data obtained in this work corroborate the hypothesis that TNF-α, CXCL-1 and IL-β cause, in addition to hyperalgesia, the release of endogenous substances such as opioid peptides, which in turn exert endogenous control over peripheral inflammatory pain.Copyright © 2021 Elsevier B.V. All rights reserved.

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