ntense Acute Swimming Induces Delayed-Onset Muscle Soreness Dependent on Spinal Cord Neuroinflammatio

Autor(es):Mostrar menos -

Borghi, Sergio M. ^{[1, 2]} ; Bussulo, Sylvia K. D. ^[2] ; Pinho-Ribeiro, Felipe A. ^[1] ; Fattori, Victor ^[1] ; Carvalho, Thacyana T. ^[1] ; Rasquel-Oliveira, Fernanda S. ^[1] ; Zaninelli, Tiago H. ^[1] ; Ferraz, Camila R. ^[1] ; Casella, Antonio M. B. ^[3] ; Cunha, Fernando Q. ^[4] ; Cunha, Thiago M. ^[4] ; Casagrande, Rubia ^[5] ; Verri Jr, Waldiceu A. A.

Afiliação do(s) autor(es)

^[1] Univ Estadual Londrina, Dept Ciencias Patol, Ctr Ciencias Biol, Londrina, Parana - Brazil

^[2] Univ Norte Parana, Ctr Pesquisa Ciencias Saude, Londrina, Parana - Brazil

^[3] Univ Estadual Londrina, Ctr Ciencias Saude, Dept Clin Med, Londrina, Parana - Brazil

^[4] Univ Sao Paulo, Dept Farmacol, Fac Med Ribeirao Preto, Sao Paulo - Brazil

^[5] Univ Estadual Londrina, Hosp Univ, Ctr Ciencias Saude, Dept Ciencias Farmaceut, Londrina, Parana - Brazil

• Tipo de documento: Artigo Científico
• Fonte: FRONTIERS IN PHARMACOLOGY; v. 12, JAN 7 2022.
• Citações Web of Science: 0

Resumo

Unaccustomed exercise involving eccentric contractions, high intensity, or long duration are recognized to induce delayed-onset muscle soreness (DOMS). Myocyte damage and inflammation in affected peripheral tissues contribute to sensitize muscle nociceptors leading to muscle pain. However, despite the essential role of the spinal cord in the regulation of pain, spinal cord neuroinflammatory mechanisms in intense swimming-induced DOMS remain to be investigated. We hypothesized that spinal cord neuroinflammation contributes to DOMS. C57BL/6 mice swam for 2 h to induce DOMS, and nociceptive spinal cord mechanisms were evaluated. DOMS triggered the activation of astrocytes and microglia in the spinal cord 24 h after exercise compared to the sham group. DOMS and DOMS-induced spinal cord nuclear factor kappa B (NF kappa B) activation were reduced by intrathecal treatments with glial inhibitors (fluorocitrate, alpha-aminoadipate, and minocycline) and NF kappa B inhibitor {[}pyrrolidine dithiocarbamate (PDTC)]. Moreover, DOMS was also reduced by intrathecal treatments targeting C-X-3-C motif chemokine ligand 1 (CX(3)CL1), tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1 beta or with recombinant IL-10. In agreement, DOMS induced the mRNA and protein expressions of CX(3)CR1, TNF-alpha, IL-1 beta, IL-10, c-Fos, and oxidative stress in the spinal cord. All these immune and cellular alterations triggered by DOMS were amenable by intrathecal treatments with glial and NF kappa B inhibitors. These results support a role for spinal cord glial cells, via NF kappa B, cytokines/chemokines, and oxidative stress, in DOMS. Thus, unveiling neuroinflammatory mechanisms by which unaccustomed exercise induces central sensitization and consequently DOMS. (AU)

• Processo FAPESP: 13/08216-2 - CPDI - Centro de Pesquisa em Doenças Inflamatórias
• Beneficiário: Fernando de Queiroz Cunha
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs