Document Detail

Melatonin reduces cardiac inflammatory injury induced by acute exercise.
MedLine Citation:
PMID:  19627457     Owner:  NLM     Status:  MEDLINE    
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.
C Veneroso; María J Tuñón; Javier González-Gallego; Pilar S Collado
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Publication Detail:
Type:  Journal Article     Date:  2009-07-13
Journal Detail:
Title:  Journal of pineal research     Volume:  47     ISSN:  1600-079X     ISO Abbreviation:  J. Pineal Res.     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-08-19     Completed Date:  2009-11-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8504412     Medline TA:  J Pineal Res     Country:  Denmark    
Other Details:
Languages:  eng     Pagination:  184-91     Citation Subset:  IM    
Institute of Biomedicine, University of León, 24071-León, Spain.
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MeSH Terms
Cardiomyopathies / drug therapy*,  etiology,  metabolism,  pathology
Cyclooxygenase 2 / genetics,  metabolism
Disease Models, Animal
Inflammation / drug therapy*,  etiology,  metabolism,  pathology
Intercellular Adhesion Molecule-1 / genetics,  metabolism
Interleukins / genetics,  metabolism
Melatonin / pharmacology*
Myocardium / metabolism,  pathology
NF-kappa B / genetics,  metabolism
Nitric Oxide Synthase Type II / genetics,  metabolism
Peroxidase / metabolism
Physical Exertion / drug effects*,  physiology
Rats, Wistar
Signal Transduction / drug effects
Tumor Necrosis Factor-alpha / genetics,  metabolism
Reg. No./Substance:
0/Interleukins; 0/NF-kappa B; 0/Tumor Necrosis Factor-alpha; 126547-89-5/Intercellular Adhesion Molecule-1; 73-31-4/Melatonin; EC; EC Oxide Synthase Type II; EC protein, rat; EC 2; EC protein, rat

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