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Oxid Med Cell Longev. 2014;2014:925981. doi: 10.1155/2014/925981. Epub 2014 Feb 6.

Anti-inflammatory effect of recreational exercise in TNBS-induced colitis in rats: role of NOS/HO/MPO system.

Author information

  • 1Department of Physiology, Anatomy and Neuroscience, University of Szeged, Közép Fasor 52, Szeged 6726, Hungary.
  • 2Institute of Physical Education and Sport Sciences, University of Szeged, Szeged 6725, Hungary ; Institute of Biochemistry, Biological Research Centre of the Hungarian Academy of Sciences, Szeged 6726, Hungary.
  • 3Institute of Biochemistry, Biological Research Centre of the Hungarian Academy of Sciences, Szeged 6726, Hungary.
  • 4AVIDIN Ltd., Szeged 6726, Hungary ; Institute of Genetics, Biological Research Center of the Hungarian Academy of Sciences, Szeged 6726, Hungary.
  • 5University of Szeged, Faculty of Dentistry and Department of Orthodontics and Pediatric Dentistry, Szeged 6720, Hungary.
  • 6AVIDIN Ltd., Szeged 6726, Hungary.
  • 7Semmelweis University, Faculty of Physical Education and Sport Sciences, Budapest 1123, Hungary.
  • 8Department of Cardiology, Medical University of Vienna, 1090 Wien, Austria.

Abstract

There are opposite views in the available literature: Whether physical exercise has a protective effect or not on the onset of inflammatory bowel disease (IBD). Therefore, we investigated the effects of recreational physical exercise before the induction of colitis. After 6 weeks of voluntary physical activity (running wheel), male Wistar rats were treated with TNBS (10 mg). 72 hrs after trinitrobenzene sulphonic acid (TNBS) challenge we measured colonic gene (TNF-α, IL-1β, CXCL1 and IL-10) and protein (TNF-α) expressions of various inflammatory mediators and enzyme activities of heme oxygenase (HO), nitric oxide synthase (NOS), and myeloperoxidase (MPO) enzymes. Wheel running significantly increased the activities of HO, constitutive NOS (cNOS) isoform. Furthermore, 6 weeks of running significantly decreased TNBS-induced inflammatory markers, including extent of lesions, severity of mucosal damage, and gene expression of IL-1β, CXCL1, and MPO activity, while IL-10 gene expression and cNOS activity were increased. iNOS activity decreased and the activity of HO enzyme increased, but not significantly, compared to the sedentary TNBS-treated group. In conclusion, recreational physical exercise can play an anti-inflammatory role by downregulating the gene expression of proinflammatory mediators, inducing anti-inflammatory mediators, and modulating the activities of HO and NOS enzymes in a rat model of colitis.

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