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目的建立常规和低脂Lieber-DeCarli液体饲料诱导的酒精性肝损伤小鼠模型。方法健康雄性昆明小鼠50只,随机分为5组(n=10),即颗粒饲料组、常规对照组、常规乙醇组、低脂对照组和低脂乙醇组。各组小鼠分别喂饲相应的饲料4周,记录每日液体饲料消耗量。4周末处死小鼠,测定血清转氨酶的活性、血清和肝脏甘油三酯(TG)的含量。制备肝脏冰冻切片,苏丹Ⅲ染色观察肝细胞脂肪变性。结果造模过程中,常规和低脂乙醇组小鼠乙醇摄入量分别为24～34 g/kg.bw/d和15～25 g/kg.bw/d。造模结束时,两液体饲料对照组小鼠体重略高于颗粒饲料组小鼠体重;两乙醇组小鼠肝脏系数均显著高于各自对照组小鼠的肝脏系数(P<0.01)。生化结果显示,常规乙醇组小鼠血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)的活性以及血清和肝脏TG含量均显著高于常规对照组水平(P<0.01);低脂乙醇组小鼠血清ALT的活性和肝脏TG含量均显著高于低脂对照组水平(P<0.05)。病理检查结果显示,乙醇组小鼠肝脏切片中有大量脂滴蓄积。结论自行配制常规和低脂液体饲料,喂饲小鼠4周,均可诱导小鼠出现酒精性肝损伤。该模型简单方便,可用于酒精性肝损伤分子机制研究和防治药物的筛选。
Objective To establish a mouse model of alcoholic liver injury induced by conventional and low-fat Lieber-DeCarli liquid diet. Methods Fifty healthy male Kunming mice were randomly divided into five groups (n = 10), namely the pellet feed group, the conventional control group, the conventional ethanol group, the low fat control group and the low fat ethanol group. Each group of mice were fed the corresponding feed for 4 weeks, record the daily liquid feed consumption. Mice were sacrificed at the end of 4 weeks to determine serum aminotransferase activity, serum and liver triglyceride (TG) levels. Frozen liver sections were prepared and stained with Sudan Ⅲ to observe the fatty degeneration of hepatocytes. Results In the process of modeling, ethanol intake of mice in conventional and low-fat group were 24-34 g / kg.bw / d and 15-25 g / kg.bw / d, respectively. At the end of modeling, the body weight of mice in the two liquid feed control groups was slightly higher than that of the control group. The hepatic coefficients of two ethanol groups were significantly higher than those of the control mice (P <0.01). The biochemical results showed that the activity of serum ALT and AST and the content of TG in serum and liver were significantly higher in conventional ethanol group than those in the control group (P <0.01) The activity of serum ALT and the content of liver TG in alcohol group mice were significantly higher than those in low-fat control group (P <0.05). Pathological examination showed that a large amount of lipid droplets accumulate in the ethanol liver slices of mice. Conclusion Both conventional and low-fat liquid diet can be formulated to induce alcoholic liver injury in mice by feeding for 4 weeks. The model is simple and convenient and can be used to study the molecular mechanism of alcoholic liver injury and the screening of prevention and treatment drugs.