Melatonin reduces cardiac inflammatory injury induced by acute exercise.
Cardiac muscle tissue, when stimulated by acute exercise, presents increased signs of cell damage. This study was designed to investigate whether overexpression of inflammatory mediators induced in the heart by acute exercise could be prevented by melatonin and whether the protective effect of melatonin was related with inhibition of nuclear factor kappa B (NF-kappaB) activation. Male Wistar rats received melatonin i.p. at a dose of 1.0 mg/kg body weight 3 min before being exercised for 60 min on a treadmill at a speed of 25 m/min and a 10% slope. Exercise was associated with a significant increase in myeloperoxidase activity and in TNF-alpha, IL-1 and IL-6 mRNA levels. Both mRNA level and protein concentrations of intercellular adhesion molecule-1, inducible nitric oxide synthase, and cyclooxygenase-2 were also significantly elevated. A significant activation of nuclear factor kappa B (NF-kappaB) was observed in exercised rats. These effects were totally or partially prevented by melatonin administration. Data obtained indicate that melatonin protects against heart damage caused by acute exercise. Impaired production of noxious mediators involved in the inflammatory process and down-regulation of the NF-kappaB signal transduction pathway appear to contribute to the beneficial effects of melatonin.
Veneroso
C
C
Institute of Biomedicine, University of León, León, Spain.
Tuñón
María J
MJ
Institute of Biomedicine, University of León, León, Spain.
González-Gallego
Javier
J
Institute of Biomedicine, University of León, León, Spain.
Collado
Pilar S
PS
Institute of Biomedicine, University of León, León, Spain.
D000818:Animals; D009202:Cardiomyopathies / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D007249:Inflammation / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D007378:Interleukins / Q000235:genetics / Q000378:metabolism; D008297:Male; D008550:Melatonin / Q000494:pharmacology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D005082:Physical Exertion / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D007378:Interleukins; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D009195:Peroxidase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D008550:Melatonin