Ozcelik Eda, Uslu Sema, Erkasap Nilufer, Karimi Hadi
Department of Nutrition and Dietetics, School of Healthy Sciences, Artvin Coruh University, Artvin, Turkey.
Department of Biochemistry, School of Medicine, Eskisehir Osmangazi University, Eskişehir, Turkey.
Kaohsiung J Med Sci. 2014 Jun;30(6):286-90. doi: 10.1016/j.kjms.2014.02.003. Epub 2014 Apr 3.
Acetaminophen (APAP) is the most commonly reported toxic ingestion in the world. Severe liver injury resulting from overdose or chronic use of APAP remains a significant clinical problem. In recent years, the mechanisms underlying liver injury caused by APAP have become much better understood. We have studied the protective effect of chitosan supplementation against APAP-induced hepatotoxicity with respect to changes in the levels of total and lipid-bound sialic acid in the serum and in the liver tissue and changes in the activity of diagnostic marker enzymes, lipid peroxidation, and ceruloplasmin oxidase enzyme in normal and experimental groups of rats. During the experimental period, chitosan (200 mg/kg body weight per day) was administered to APAP + chitosan-treated rats by oral gavage. Results showed that treatment with APAP induced a significant increase in the serum alanine aminotransferase and alkaline phosphatase activities, in total and lipid-bound sialic acids levels, and in the liver lipid peroxide content. The administration of chitosan significantly prevented APAP-induced alterations in the levels of diagnostic marker enzymes, total sialic acid, lipid-bound sialic acid, and malondialdehyde in the experimental groups of rats. Furthermore, chitosan administration increased the activity of ceruloplasmin oxidase. In conclusion, our results suggest that chitosan has a protective effect on APAP-induced hepatic injury in rats. The study sheds light on the therapeutic potential of chitosan in an APAP-induced hepatotoxicity model.
对乙酰氨基酚(APAP)是全球报告中最常见的有毒摄入物。过量服用或长期使用APAP导致的严重肝损伤仍是一个重大临床问题。近年来,APAP所致肝损伤的潜在机制已得到更好的理解。我们研究了壳聚糖补充剂对APAP诱导的肝毒性的保护作用,涉及正常组和实验组大鼠血清及肝组织中总唾液酸和脂质结合唾液酸水平的变化,以及诊断标志物酶活性、脂质过氧化和铜蓝蛋白氧化酶的变化。在实验期间,通过口服灌胃给APAP + 壳聚糖处理组的大鼠给予壳聚糖(每天200 mg/kg体重)。结果显示,APAP处理导致血清丙氨酸转氨酶和碱性磷酸酶活性、总唾液酸和脂质结合唾液酸水平以及肝脏脂质过氧化物含量显著增加。壳聚糖给药显著预防了APAP诱导的大鼠实验组诊断标志物酶、总唾液酸、脂质结合唾液酸和丙二醛水平的改变。此外,壳聚糖给药增加了铜蓝蛋白氧化酶的活性。总之,我们的结果表明壳聚糖对APAP诱导的大鼠肝损伤具有保护作用。该研究揭示了壳聚糖在APAP诱导的肝毒性模型中的治疗潜力。