非酒精性脂肪肝病模型 z-bio 2021-07-26 530

　　Objective: To establish a model of non-alcoholic fatty liver disease with a new type of hyperlipidemia-sensitive rats, observe the changes in blood biochemical indicators and pathological properties, explore its application and scientific research value, and provide new options to become an animal model of AFLD disease.

　　Method 20 WSHc rats aged 7-8 weeks were randomly divided into two groups, fed with a normal diet and a high-fat diet. Another 20 Wistar rats of the same age were treated in the same way as this group. After 12 weeks of continuous feeding, serum TC, TG, ALT, AST levels were detected and elastic ultrasound imaging was performed. After the animals were slaughtered, the liver was harvested for HE, Oil Red O, Masson and immunofluorescence staining. Observe the liver morphology, lipid deposition, inflammation and fibrosis in each group. The liver of WSHc rats after a high-fat diet. The characteristics of the lesion.

　　Compared with Wistar rats fed a high-fat diet, high-fat induced WSHc rats, serum total cholesterol was significantly increased, similar to clinical hyperlipidemia patients; liver lipid abnormalities. Deposited in bullous lipid droplets: inflammatory cells infiltrate the surrounding area, lipid droplets form inflammatory foci, there are many macrophages, and scattered fibrous lesions can be seen. However, these pathological changes were not observed in the liver tissue of Wistar rats induced by high fat.

　　Conclusion Compared with Wistar rats, the blood lipids and liver enzymes of WSHc rats are close to clinical levels after hyperlipidemia is induced. Lipid deposition and inflammation in liver tissue are more serious, and liver cirrhosis may be scattered. As a new and ideal NAFLD animal model.