大鼠酒精性脂肪肝模型的建立

Establishment of rat fatty liver model induced by alcohol

目的探索一种相对简单可靠的方法制作大鼠酒精性脂肪肝模型。方法采用乙醇灌胃法结合高脂饮食,在6周时间内建立酒精性脂肪肝模型。HE染色观察肝脏病理学改变;全自动生化分析仪分析血清谷丙转氨酶(ALT)、谷草转氨酶(AST)活性,总胆红素(TBIL)、总胆固醇(TC)、甘油三酯(TG)含量;生化法测定肝匀浆超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)活性以及丙二醛(MDA)含量、肝脏甘油三酯(TG)水平。结果 6周末,酒精引起了明显的肝脏脂肪变性;血清ALT活性以及TBIL、TG水平升高;肝匀浆SOD、GPx活性降低,MDA含量升高;肝组织TG含量升高。结论采用高脂饮食结合酒精灌胃法,可成功制作大鼠酒精性脂肪肝模型。

Objective To establish a relatively simple and feasible rat model of alcoholic fatty liver. Methods Rat model of alcoholic fatty liver was induced by intragastfic infusion of ethanol and high-fat diet for six weeks. Histopathological changes of live were assessed by hematoxylin and eosin staining. The activities of alanine transarninase（ALT） and aspartate aminotransferase（ AST）, the levels of total bilirubin（ TBIL）, total cholesterol（TC） and triglycefide（TG） in serum were detected with routine laboratory methods using an autoana- lyzer. The activities of superoxide dismutase （SOD） and glutathione peroxidase（GPx） and the level of malondialdehyde （MDA） in liver homogenates were measured by spectrophotometry. The TG content in liver tissue was determined by spectrophotometry. Results At the end of the experiment, alcohol could induce liver injury as evidenced by aggravated steatosis, increased activity of ALT and levels of TBIL and TG in serum, reduced SOD and GPx activities and elevated MDA content in liver homogenates and TG content in liver tissue. Conclasion Alcoholic fatty liver model in rat was successfully established by alcohol garage and high fat diet.