Shokrzadeh Mohammad, Ahmadi Amirhossein, Naghshvar Farshad, Chabra Aroona, Jafarinejhad Mehdi
Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Mazandaran University of Medical Sciences, 18 Kilometers of Farah Abad Road, Sari 48175-861, Iran ; Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, 18 Kilometers of Farah Abad Road, Sari 48175-861, Iran.
Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Mazandaran University of Medical Sciences, 18 Kilometers of Farah Abad Road, Sari 48175-861, Iran.
Biomed Res Int. 2014;2014:470425. doi: 10.1155/2014/470425. Epub 2014 Jun 30.
The current study aimed to evaluate the protective effects of melatonin, a pineal secretory product, against hepatotoxicity induced by cyclophosphamide (CP) in mice. Mice were pretreated with melatonin intraperitoneally for 7 consecutive days before the administration of a single intraperitoneal dose of 200 mg/kg CP. 24 hr after CP administration, the mice were anesthetized, blood was then removed, and serum toxicity enzymes activities were evaluated. After the blood sampling, all animals were killed, livers were then removed, and histological studies were conducted. Serum toxicity marker enzymes were significantly increased after CP treatment but restored in melatonin pretreated groups. In addition, administration of CP induced necrotic hepatocyte with small crushed nuclei, portal space with severe inflammation, and hepatocytes surrounded by lymphocytic infiltration in hepatic tissues. However, melatonin effectively protected against CP-induced histopathological abnormalities in the liver tissues. Our results reveal that melatonin produces a potent hepatoprotective mechanism against CP. Therefore, melatonin could be a potent candidate to use concomitantly as a supplement agent against hepatotoxicity of CP for the patients undergoing chemotherapy.
本研究旨在评估松果体分泌产物褪黑素对环磷酰胺(CP)诱导的小鼠肝毒性的保护作用。在单次腹腔注射200mg/kg CP前,小鼠连续7天腹腔注射褪黑素进行预处理。CP给药24小时后,将小鼠麻醉,取血并评估血清毒性酶活性。采血后,处死所有动物,取出肝脏并进行组织学研究。CP处理后血清毒性标志物酶显著升高,但在褪黑素预处理组中恢复。此外,CP给药导致肝组织中出现坏死的肝细胞,细胞核小且破碎,门管区有严重炎症,肝细胞周围有淋巴细胞浸润。然而,褪黑素有效保护了肝脏组织免受CP诱导的组织病理学异常。我们的结果表明,褪黑素对CP产生了强大的肝保护机制。因此,褪黑素可能是一种有效的候选药物,可作为辅助剂与正在接受化疗的患者同时使用,以对抗CP的肝毒性。