[摘要]目的：通过改良的高糖高脂饮食建立非酒精性脂肪肝C57BL/6J小鼠模型。方法：取健康雄性小鼠，随机分为两组：对照组，普通饲料喂养；实验组（NAFLD组），高脂饮食喂养。构建非酒精性脂肪肝模型。喂养12周，每周记录摄食量和体重，第12周检测小鼠脂肪垫重量、肝指数和脂肪指数，取肝脏组织，进行病理学观察。结果：从第二周开始，NAFLD组摄食量较对照组差距逐渐增大。第12周对照组体重增加比NAFLD组显著降低。NAFLD模型组脂肪垫总重量与脂肪指数明显大于对照组（P<0.05）。NAFLD模型组肝指数均高于对照组（P<0.05）。NAFLD模型组，肝细胞出现脂肪病变，细胞核坏死，细胞间质有炎细胞聚集，炎症反应明显高于对照组（P<0.05）。结论：在高脂饮食的诱导下成功建立小鼠非酒精性脂肪肝模型。
[关键词]非酒精性脂肪肝；高脂饮食；小鼠模型；
[ABSTRACT] Objective The mouse model of nonalcoholic fatty liver was induced by modified high-fat diet to further explore its pathogenesis and new therapeutic targets. MethodMale healthy mice were randomly assigned to two groups: control group, fed with ordinary diet; The experimental group (NAFLD group) was fed with high-fat diet. The model of nonalcoholic fatty liver was established. After feeding for 12 weeks, the diet and body weight were recorded every week. At the 12th week, the weight of fat pad, liver index and fat index were measured. The liver tissue was taken for pathological observation. Results From the second week, the difference in food intake between NAFLD group and control group gradually increased. At the 12th week, the weight gain in the control group was significantly less than that in the NAFLD group. The total weight and fat index of fat pad in NAFLD model group were significantly more than those in control group (P < 0.05). The liver index in NAFLD model group was more than that in control group (P < 0.05). In NAFLD model group, hepatocytes showed fatty lesions, nuclear necrosis, inflammatory cell aggregation in intercellular matrix, and the inflammatory reaction was significantly higher than that in the control group (P < 0.05). Conclusion The results showed that the model of nonalcoholic fatty liver in mice was successfully established under the induction of high-fat diet.
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