Akademik Veri Yönetim Sistemi
Namık Kemal Tıp Dergisi, cilt.12, ss.1-10, 2023 (Hakemli Dergi)
Aim: Myocardial infarctus (MI) causes myocardial edema but its association with aquaporin (AQP) channels and effects of melatonin (MEL) on that are not well known. Therefore, aim of the current study was to investigate effects of MEL on myocardial edema and gene expression AQP channels on rat model of MI.
Methods: In Wistar rats, MI model was established with 85mg/kg isoproterenol. A total of 28 rats were divided into four groups as: Control, Isoproterenol (ISO), Melatonin (MEL), and Isoproterenol+Melatonin (ISOMEL). MEL group were administered 10mg/kg MEL for 7 days. On day 7, ECG 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 evaluation of edema and mononuclear 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 aquaporine channels, suggesting that it could potentially be used to ameliorate the effects of MI.