Melatonin Reduces Cardiac Injury Induced by Lipopolysaccharides in Rats
Journal Title: Journal of Medical Science And clinical Research - Year 2014, Vol 2, Issue 10
Abstract
Lipopolysaccharide (LPS) is known to cause inflammation and switch myocardial fuel similar to that of the failing heart: reduced mitochondrial substrate flux and myocyte lipid accumulation. The nuclear receptor: peroxisome proliferator activated receptor-alpha (PPARα) and PPAR-gamma coactivator-1alpha (PGC-1α) play important roles in transcriptional regulation of myocardial metabolism and may contribute to the changes that accompanied cardiomyopathic alterations in chronic inflammation. Melatonin is claimed to have antiinflammatory activity in animal models. Our work was designed to assess the modulatory effect of melatonin on LPS-induced lipotoxic effect in heart of male albino rats for 6weeks. A systemic vehicle or LPS alone or combined with melatonin was administered. Serum cardiac enzymes, cardiac lipids and 3-nitrotyrosin (3-NT) and the gene expression of cardiac nuclear factor-kappa B (NF-κB), PPARα and PGC-1α were measured. Melatonin treatment showed a significant improvement of cardiac enzymes together with reduced cardiac lipid accumulation, 3-NT and NF-κβ and PPARα that paralleled enhancement of PGC-1α gene expression compared with the LPS rats.We conclude that cardioprotection of melatonin in chronic inflammatory condition is related to restoration of PGC-1α expression in addition to its antioxidant and anti-inflammatory capacity.
Authors and Affiliations
Ola M. Tork
Keywords
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