Melatonin is thought to have the ability of antiatherogenic,
antioxidant, and vasodilatory. It is not only a promising protective in acute
myocardial infarction but is also a useful tool in the treatment of pathological remodeling. However, its role in myocardial
hypertrophy remains unclear. In this study, we investigated the protective effects of
melatonin on myocardial
hypertrophy induced by
lipopolysaccharide (LPS) and to identify their precise mechanisms. The cultured myocardial cell was divided into six groups: control group, LPS group, LPS +
ethanol (4%), LPS +
melatonin (1.5 mg/ml) group, LPS +
melatonin (3 mg/ml) group, and LPS +
melatonin (6 mg/ml) group. The morphologic change of myocardial cell was observed by inverted phase contrast microscope. The
protein level of myocardial cell was measured by
Coomassie brilliant blue protein kit. The secretion level of
tumor necrosis factor-α (TNF-α) was evaluated by
enzyme-linked
immunosorbent assay (ELISA). Ca(2+) transient in
Fura-2/AM-loaded cells was measured by Till image system. The expression of Ca(2+)/
calmodulin-dependent
kinase II (
CaMKII) and
calcineurin (CaN) was measured by Western blot analysis. Our data demonstrated that LPS induced myocardial
hypertrophy, promoted the secretion levels of TNF-α, and increased Ca(2+) transient level and the expression of
CaMKII and CaN. Administration of
melatonin 30 min prior to LPS stimulation dose-dependently attenuated myocardial
hypertrophy. In conclusion, the results revealed that
melatonin had the potential to protect against myocardial
hypertrophy induced by LPS in vitro through downregulation of the TNF-α expression and retains the intracellular Ca(2+) homeostasis.