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Diclofenac pretreatment effects on the toll-like receptor 4/nuclear factor kappa B-mediated inflammatory response to eccentric exercise in rat liver

dc.contributor.authorBarcelos R.P.
dc.contributor.authorBresciani G.
dc.contributor.authorRodriguez-Miguelez P.
dc.contributor.authorCuevas M.J.
dc.contributor.authorSoares F.A.A.
dc.contributor.authorBarbosa N.V.
dc.contributor.authorGonzález-Gallego J.
dc.date.accessioned2020-09-02T22:12:58Z
dc.date.available2020-09-02T22:12:58Z
dc.date.issued2016
dc.identifier10.1016/j.lfs.2016.02.006
dc.identifier.citation148, , 247-253
dc.identifier.issn00243205
dc.identifier.urihttps://hdl.handle.net/20.500.12728/3676
dc.descriptionAcute 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 (10 mg/kg) for 7 days 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. © 2016 Elsevier Inc. All rights reserved.
dc.language.isoen
dc.publisherElsevier Inc.
dc.subjectAcute exercise
dc.subjectDiclofenac
dc.subjectInflammation
dc.subjectLiver
dc.subjectNF-κB
dc.subjectTLR4
dc.subjectdiclofenac
dc.subjectI kappa B
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinducible nitric oxide synthase
dc.subjectinterleukin 6
dc.subjectmessenger RNA
dc.subjectmyeloid differentiation factor 88
dc.subjecttoll like receptor 4
dc.subjecttoll like receptor adaptor molecule 1
dc.subjecttranscription factor RelA
dc.subjecttumor necrosis factor alpha
dc.subjectautacoid
dc.subjectdiclofenac
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectTlr4 protein, rat
dc.subjecttoll like receptor 4
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectcell differentiation
dc.subjectcontrolled study
dc.subjecteccentric exercise
dc.subjectexercise
dc.subjectexercise induced liver inflammation
dc.subjectexercise induced liver inflammation
dc.subjectexperimental hepatitis
dc.subjectgene expression
dc.subjectmale
dc.subjectnonhuman
dc.subjectnucleotide sequence
dc.subjectprotein expression
dc.subjectrat
dc.subjectreal time polymerase chain reaction
dc.subjecttreatment duration
dc.subjectupregulation
dc.subjectWestern blotting
dc.subjectanimal
dc.subjectantagonists and inhibitors
dc.subjectdrug effects
dc.subjectliver
dc.subjectmetabolism
dc.subjectphysiology
dc.subjecttreatment outcome
dc.subjectWistar rat
dc.subjectAnimals
dc.subjectDiclofenac
dc.subjectInflammation Mediators
dc.subjectLiver
dc.subjectMale
dc.subjectNF-kappa B
dc.subjectPhysical Conditioning, Animal
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectToll-Like Receptor 4
dc.subjectTreatment Outcome
dc.titleDiclofenac pretreatment effects on the toll-like receptor 4/nuclear factor kappa B-mediated inflammatory response to eccentric exercise in rat liver
dc.typeArticle


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