Peizhu Tan1,2, Huan Liang1,2,3, Junhui Nie1,2, Yan Diao1,2, Qi He1,2, Baoyu Hou1,2, Tingting Zhao1,2, Hui Huang1,2, Yanze Li1,2, Xu Gao1,2, Lingyun Zhou1,2, Ying Liu4. 1. a Department of Biochemistry and Molecular Biology , Harbin Medical University , Harbin , China. 2. b Translational Medicine Center of Northern China , Harbin , China. 3. c Department of Clinical Laboratory , Harbin Medical University Cancer Hospital , Harbin , China. 4. d Department of Gastroenterology , Heilongjiang Province Hospital , Harbin , China.
Abstract
BACKGROUND: Alcoholic fatty liver disease (AFLD) defines an important stage in the progression of alcoholic liver disease (ALD), which is a major cause of morbidity and mortality worldwide. OBJECTIVE: To establish a mouse model of AFLD. METHODS: Male C57BL/6 mice were divided into the following two groups: (i) a control group, which was allowed free access to food and water and (ii) an alcohol-treated group, which was administered a 15% (v/v) alcohol solution instead of water. After 8-9 months of treatment, serum biochemical indexes, histopathological changes, liver triglyceride content, iron storage, and ferritin light chain protein expression were measured using an automatic biochemical analyzer, hematoxylin-eosin (HE) staining, a commercially available kit, Prussian blue staining, and Western blot analysis, respectively. RESULTS: Compared with the control group, the alcohol-treated group displayed increased levels of serum LDH, ALT, and AST, decreased levels of ALB, and no significant change in levels of TP. Additionally, increased levels of serum TG, T-CHO, and LDL and decreased levels of serum GLU and HDL were observed in the alcohol-treated mice. HE staining showed that lipid vacuolization occurred in the livers of alcohol-treated mice. The alcohol-treated mice also exhibited increased liver triglyceride content. Moreover, Prussian blue staining and Western blot analysis demonstrated that chronic alcohol administration caused iron overloading of the liver. CONCLUSIONS: Chronic administration of 15% (v/v) alcohol in the drinking water over 8-9 months caused AFLD in mice. Our results establish an AFLD model that represents a promising tool for the future study of the progression of ALD.
BACKGROUND:Alcoholic fatty liver disease (AFLD) defines an important stage in the progression of alcoholic liver disease (ALD), which is a major cause of morbidity and mortality worldwide. OBJECTIVE: To establish a mouse model of AFLD. METHODS: Male C57BL/6 mice were divided into the following two groups: (i) a control group, which was allowed free access to food and water and (ii) an alcohol-treated group, which was administered a 15% (v/v) alcohol solution instead of water. After 8-9 months of treatment, serum biochemical indexes, histopathological changes, liver triglyceride content, iron storage, and ferritin light chain protein expression were measured using an automatic biochemical analyzer, hematoxylin-eosin (HE) staining, a commercially available kit, Prussian blue staining, and Western blot analysis, respectively. RESULTS: Compared with the control group, the alcohol-treated group displayed increased levels of serum LDH, ALT, and AST, decreased levels of ALB, and no significant change in levels of TP. Additionally, increased levels of serum TG, T-CHO, and LDL and decreased levels of serum GLU and HDL were observed in the alcohol-treated mice. HE staining showed that lipid vacuolization occurred in the livers of alcohol-treated mice. The alcohol-treated mice also exhibited increased liver triglyceride content. Moreover, Prussian blue staining and Western blot analysis demonstrated that chronic alcohol administration caused iron overloading of the liver. CONCLUSIONS: Chronic administration of 15% (v/v) alcohol in the drinking water over 8-9 months caused AFLD in mice. Our results establish an AFLD model that represents a promising tool for the future study of the progression of ALD.