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Appl Physiol Nutr Metab. 2017 Jul;42(7):757-764. doi: 10.1139/apnm-2016-0593. Epub 2017 Feb 24.

Diclofenac pretreatment modulates exercise-induced inflammation in skeletal muscle of rats through the TLR4/NF-κB pathway.

Author information

1
a Programa de Pós-graduação em Bioexperimentação, Universidade de Passo Fundo, RS, 99052-900, Brazil.
2
c Institute of Biomedicine, University of León, Campus Universitario, 24071 León, Spain.
3
d Programa de Pós-Graduação em Bioquímica Toxicológica, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900 Brazil.
4
b Grupo de Investigación en Rendimiento Físico y Salud Escuela de Educación Física, Pontificia Universidad Católica de Valparaiso, Valparaiso, 2530388 Chile.
5
e Programa de Pós-Graduação em Bioquímica Toxicológica, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil.

Abstract

Nonsteroidal anti-inflammatory drugs, such as diclofenac, are widely used to treat inflammation and pain in several conditions, including sports injuries. This study analyzes the influence of diclofenac on the toll-like receptor-nuclear factor kappa B (TLR-NF-κB) pathway in skeletal muscle of rats submitted to acute eccentric exercise. Twenty male Wistar rats were divided into 4 groups: control-saline, control-diclofenac, exercise-saline, and exercise-diclofenac. Diclofenac or saline were administered for 7 days prior to an acute eccentric exercise bout. The inflammatory status was evaluated through mRNA levels of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), IL-1β, and tumor necrosis factor alpha (TNF-α), and protein content of COX-2, IL-6, and TNF-α in vastus lateralis muscle. Data obtained showed that a single bout of eccentric exercise significantly increased COX-2 gene expression. Similarly, mRNA expression and protein content of other inflammation-related genes also increased after the acute exercise. However, these effects were attenuated in the exercise + diclofenac group. TLR4, myeloid differentiation primary response gene 88 (MyD88), and p65 were also upregulated after the acute eccentric bout and the effect was blunted by the anti-inflammatory drug. These findings suggest that pretreatment with diclofenac may represent an effective tool to ameliorate the pro-inflammatory status induced by acute exercise in rat skeletal muscle possibly through an attenuation of the TLR4-NF-κB signaling pathway.

KEYWORDS:

AINS; COX; NF-κB; NSAIDs; eccentric exercise; exercice pliométrique; inflammation; muscle squelettique; skeletal muscle

PMID:
28235185
DOI:
10.1139/apnm-2016-0593
[Indexed for MEDLINE]

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