Suzuki H, Tominaga T, Mizuno H, Kouno M, Suzuki M, Kato Y, Sato A, Okabe K, Uchikoshi T, Maezono K
Department of Internal Medicine, St. Marianna University School of Medicine, Yokohama, Japan.
Alcohol Alcohol Suppl. 1993;1A:111-7. doi: 10.1093/alcalc/28.supplement_1a.111.
There is a widespread belief that when ethanol is fed to rats for a long time, it produces only fatty degeneration without necrosis or fibrosis. In this study, hydrazine sulfate, an inhibitor of low Km ALDH and gluconeogenetic enzymes, was fed with ethanol to rats, and produced more serious pathological changes compared with those found in Lieber's model. Male Sprague-Dawley rats were fed with a low fat liquid diet as a basal diet with ethanol (4%, w/v) and hydrazine sulfate for 4 weeks. At the end of the experiment, plasma aminotransferase levels were found to be elevated. Histological examination showed not only fatty degeneration but also pericellular fibrosis. Therefore, we have evaluated the curative effect of glucogenic amino acids, alanine and glutamine, on this hepatic injury model and found them to be partially protective.
人们普遍认为，长期给大鼠喂食乙醇只会导致脂肪变性，而不会出现坏死或纤维化。在本研究中，低 Km 醛脱氢酶（ALDH）和糖异生酶的抑制剂硫酸肼与乙醇一起喂给大鼠，与利伯模型相比，产生了更严重的病理变化。雄性斯普拉格-道利大鼠以低脂液体饮食作为基础饮食，同时摄入乙醇（4%，w/v）和硫酸肼，持续 4 周。实验结束时，发现血浆氨基转移酶水平升高。组织学检查显示不仅有脂肪变性，还有细胞周围纤维化。因此，我们评估了生糖氨基酸丙氨酸和谷氨酰胺对该肝损伤模型的治疗效果，发现它们具有部分保护作用。
