动物造模,脑衰老样病变模型 z-bio 2022-09-01 308

　　Objective: To induce an animal model of metabolic syndrome complicated with brain aging-like lesions in C57 mice by catch-up growth diet, and to study its possible mechanism.

　　Methods: 40 C57 mice were randomly divided into 4 groups, 10 in normal control group, 10 in low-energy diet group, 10 in high-energy diet group, and 10 in catch-up growth group (feeding on low-energy diet for 6 weeks and then on high-energy diet). The animals in each group were fed continuously for 12 weeks, the body weight and blood sugar were recorded, the metabolic syndrome-related biochemical indexes were detected at the end of the experiment, the insulin resistance index was calculated, and the expression levels of aging-related protein P53 and phosphorylated P53 (ser15) were detected by Western blot technology. The deposition of lipofuscin in the hippocampus was observed.

　　Results: The weight, blood sugar, metabolic syndrome-related biochemical indexes (serum cholesterol, triacylglycerol, insulin-like growth factor 1, insulin) and the protein expression levels of P53 and phosphorylated P53 in the low-energy group were lower than those in the normal control group. Pigmentation was less; the metabolic syndrome indexes in the high-energy group and the catch-up growth group were significantly higher than those in the control group, and the expression of P53 and phosphorylated P53 proteins increased significantly and lipofuscin deposition; the catch-up growth group showed more obvious Predisposition to insulin resistance and brain aging-like changes.

　　Conclusion: Catching-up diet feeding can induce the mouse model of metabolic syndrome complicated with brain aging-like lesions. This study provides a new research idea for the establishment of a model of metabolic syndrome and its complications neurodegeneration-like changes caused by dietary changes.