Based on the zebrafish model,the therapeutic effect of ursolic acid (UA) on non-alcoholic fatty liver disease (NAFLD) in zebrafish was explored,and the molecular mechanism of NAFLD treatment was studied.The wild type AB strain zebrafish were randomly selected and divided into normal group,model group and UA group (5,10,20 μg/mL).The normal group was given 3.5% glucose,and the model group was given 3.5% fructose for 96 h to induce a non-alcoholic fatty liver model in zebrafish.The 3.5% fructose was administered with the corresponding concentration of 5,10 and 20 μg/mL UA as the administration group,and the liquid was changed once a day.Juvenile fish were collected,and the juvenile fish body weight,body length and condition factor were used to reflect the fatness of juvenile fish.Whole oil red O staining and hematoxylin-eosin (HE) staining were used to observe the liver lipid degeneration and the degree of histopathological damage.Triglyceride and total cholesterol test kits were used to detect the body fat content of zebrafish.RT-qPCR was used to detect the expression of mTOR/SREBP-1c/ACC1/Fasn mRNA in zebrafish.Compared with the normal group,the model group had severe liver lipid deposition,and the expression levels of TG,TC,mTOR,SREBP-1c,ACC1 and Fasn mRNA in zebrafish were increased (P<0.05).Compared with the model group,the lipid deposition in the liver of zebrafish was decreased after administration,and the expressions of TG,TC and mTOR,SREBP-1c,ACC1 and Fasn mRNA were decreased (P<0.01)，which suggested that UA has a certain protective effect on NAFLD,and the mechanism may be related to regulating lipid metabolism,thereby inhibiting liver lipid synthesis.