乙醇对大鼠半乳糖胺诱导性肝炎肝毒性的增强作用：丙硫氧嘧啶的保护作用

Potentiation of hepatotoxicity by ethanol in galactosamine-induced hepatitis in rats: role of propylthiouracil protection.

作者信息

Nadkarni G D, Naik S B, Talavdekar R V, Soman C S, Talwalkar G V, Ganatra R D

出版信息

Acta Pharmacol Toxicol (Copenh). 1983 Feb;52(2):90-4. doi: 10.1111/j.1600-0773.1983.tb03408.x.

DOI:10.1111/j.1600-0773.1983.tb03408.x

Abstract

Chronic ingestion of ethanol (5 g/kg/day) for 6 weeks increased the hepatotoxicity of a single injection of D-galactosamine (330 mg/kg) in rats. Plasma transaminases, alkaline phosphatase, gamma glutamyl transpeptidase and sulphobromophthalein retention were consistently high in alcohol-fed rats compared to sucrose-fed controls, 25 hours after galactosamine administration. Liver histology in sucrose-fed rats revealed typical inflammatory changes and cytoplasmic vacuolation without cell necrosis was seen. Propylthiouracil treatment had no beneficial or protective effect in alcohol-fed rats in this animal model of hepatitis.

摘要

大鼠连续6周每天摄入乙醇（5克/千克）会增加单次注射D-半乳糖胺（330毫克/千克）后的肝毒性。与蔗糖喂养的对照组相比，在给予半乳糖胺25小时后，乙醇喂养的大鼠血浆转氨酶、碱性磷酸酶、γ-谷氨酰转肽酶和磺溴酞钠潴留水平持续偏高。蔗糖喂养大鼠的肝脏组织学显示典型的炎症变化，可见细胞质空泡化但无细胞坏死。在该肝炎动物模型中，丙硫氧嘧啶治疗对乙醇喂养的大鼠没有有益或保护作用。