Krupalija-Fazlic Mersiha, Kapic Dina, Sahinovic Maida, Custovic Samra, Muzika Visnja
Department of Dermatovenerology, Clinical Center, University of Sarajevo, Sarajevo, Bosnia and Herzegovina.
Department of Histology and Embryology, Faculty of Medicine, University of Sarajevo, Sarajevo, Bosnia and Herzegovina.
Med Arch. 2025;79(2):86-91. doi: 10.5455/medarh.2025.79.86-91.
Gentamicin is a potent, broad-spectrum aminoglycoside antibiotic used in the treatment of many infections. Gentamicin can induce hepatotoxicity through oxidative stress and apoptosis. Since melatonin has antioxidant properties, its protective effects on liver tissue damage were evaluated in this study.
The aim of this study was to conduct our investigation to assess the hepatoprotective effects of melatonin in rats treated with gentamicin.
Forty eight adult male Wistar rats were used. The animals were randomly distributed into six groups of equal size. During the period of 11 days, three control groups of rats were daily injected i.p. with the vehicle or with melatonin at a dose of 5 or 10 mg/kg. The gentamicin group was injected with gentamicin at a dose of 80 mg/kg during 8 days and vehicle for 11 days. The other two experimental groups were administered gentamicin (80 mg/kg during) 8 days and melatonin (doses of 5 and 10 mg/kg) 3 days before and 8 days concomitantly with melatonin. Obtained liver sections were analyzed using qualitative, semi-quantitative, and stereological analysis.
Gentamicin expressed hepatotoxic effects inducing congestion of lobular blood vessels, hydropic degeneration of periportal hepatocytes and mononuclear infiltration in the portal tract. Treatment with gentamicin resulted in an increase in the Vv of blood vessels, a decrease in the Vv of hepatocytes, and a decrease in the glycogen content in all three lobular zones. Melatonin administration reduced the liver alterations induced by gentamicin; the higher dose had a more potent protective effect.
Melatonin has a beneficial effect on gentamicin-induced liver damage and the effect is dose-dependent.
庆大霉素是一种强效的广谱氨基糖苷类抗生素，用于治疗多种感染。庆大霉素可通过氧化应激和细胞凋亡诱导肝毒性。由于褪黑素具有抗氧化特性，本研究评估了其对肝组织损伤的保护作用。
本研究旨在评估褪黑素对庆大霉素处理的大鼠的肝保护作用。
使用48只成年雄性Wistar大鼠。将动物随机分为六组，每组大小相等。在11天的时间里，三个对照组的大鼠每天腹腔注射溶剂或5或10mg/kg剂量的褪黑素。庆大霉素组在8天内注射80mg/kg剂量的庆大霉素，11天内注射溶剂。另外两个实验组在8天内注射庆大霉素（80mg/kg），并在注射庆大霉素前3天和同时注射8天的褪黑素（5和10mg/kg剂量）。对获得的肝脏切片进行定性、半定量和体视学分析。
庆大霉素表现出肝毒性作用，导致小叶血管充血、门周肝细胞水样变性和门管区单核细胞浸润。庆大霉素处理导致血管体积分数增加、肝细胞体积分数减少以及所有三个小叶区糖原含量减少。褪黑素给药减轻了庆大霉素诱导的肝脏改变；较高剂量具有更强的保护作用。
褪黑素对庆大霉素诱导的肝损伤具有有益作用，且该作用呈剂量依赖性。
