| Summary: | Aim:Myocardial infarction (MI) commonly results in myocardial edema, but the relationship between aquporin channels (AQP) and the effects of melatonin (MEL) on MI are not well known. Therefore, the aim of the current study was to investigate the effects of MEL on myocardial edema and the change of gene expression level of AQP channels in an experimental MI model.Materials and Methods:In this study 28 Wistar Albino male rats were used. MI model was established with isoproterenol (85mg/kg). Rats were divided into four groups as: control, isoproterenol (ISO), melatonin (MEL), and isoproterenol+melatonin (ISO+MEL). MEL group was administered 10 mg/kg MEL for 7 days. On day 8, electrocardiographic recordings and blood samples were obtained. Rats were then euthanized and left ventricle tissues were obtained. cTnI and CK-MB levels were examined to assess the success of MI model. AQP1, AQP3, AQP4, AQP7, TNF-α, BAX and Caspase-3 gene expression levels were determined. Histopathological examination was performed on left ventricle samples for the evaluation of edema and mononuclear cellular infiltration.Results:Histopathological examination and cTnl and CK-MB levels showed that MI model was produced successfully and MEL significantly reduced myocardial edema and decreased AQP1, AQP3, AQP4 and AQP7 gene expression levels.Conclusion:The results show that MEL decreases myocardial edema by reducing AQP channels, suggesting that it could potentially be used to ameliorate the effects of MI.
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