Abstract:
UNLABELLED:Acute exercise is a stress stimulus that may cause cell damage through the activation of the toll-like receptor (TLR)4 pathway, resulting in the translocation of nuclear factor kappa B (NF-κB) into the cell nucleus and the upregulation of inflammatory genes. Nonsteroidal anti-inflammatory drugs, such as diclofenac, are often prescribed to counteract exercise-induced inflammation. AIMS:This study analyzed effects of diclofenac pretreatment on the TLR4/NF-κB pathway in rat liver after an acute eccentric exercise. MAIN METHODS:Twenty male Wistar rats were divided in four groups: control-saline, control-diclofenac, exercise-saline and exercise-diclofenac. The rats received saline or diclofenac (10mg/kg) for 7days prior to an eccentric exercise bout. KEY FINDINGS:After exercise there was an increase in TLR4, myeloid differentiation primary response gene 88 (MyD88), TIR domain-containing adaptor inducing interferon (TRIF) and p65 NF-κB subunit protein levels. Exercise also resulted in increased mRNA and protein expression of interleukin (IL)-6, inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF)-α. Proinflammatory effects of exercise were prevented by the administration of diclofenac, which blunted the activation of the TLR4/NF-κB pathway and the inflammatory response in the liver of exercised rats. SIGNIFICANCE:Results from the present study highlight the role of TLR4 as a target for anti-inflammatory interventions.
journal_name
Life Scijournal_title
Life sciencesauthors
Barcelos RP,Bresciani G,Rodriguez-Miguelez P,Cuevas MJ,Soares FA,Barbosa NV,González-Gallego Jdoi
10.1016/j.lfs.2016.02.006subject
Has Abstractpub_date
2016-03-01 00:00:00pages
247-53eissn
0024-3205issn
1879-0631pii
S0024-3205(16)30056-Xjournal_volume
148pub_type
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