动物造模,糖尿病下肢溃疡小鼠模型 z-bio 2022-09-09 561

　　Objective To establish and evaluate a mouse model of diabetic lower extremity ulcer, reveal the changes of blood flow and pathophysiology in the operated limb of diabetic lower extremity ulcer mice, and explore its pathogenesis, so as to provide a basis and reference for the study of diabetic peripheral vascular disease.

　　Methods Mice were divided into lower extremity ischemia group, diabetes group and diabetic lower extremity ulcer group. Diabetic lower extremity ulcer and diabetes group were given intraperitoneal injection of streptozotocin (STZ) to establish type 1 diabetes model. Diabetic lower extremity ulcer and lower extremity ischemia group were treated with The lower extremity ischemia model was established by ligating the femoral artery and femoral vein at a high position and isolating the femoral artery. The diabetic group was only treated with sham operation. On the 0th, 3rd, 7th, 14th, and 21st days after the operation, the blood flow was monitored by laser Doppler. After 21 days, HE slices were used to observe tissue morphological changes, and the expressions of platelet-endothelial cell adhesion molecule-1 (PECAM-1/CD31) and anti-smooth muscle antibody (SMA) were analyzed.

　　Results After ischemia, compared with the lower extremity ischemia group, the diabetic lower extremity ulcer group had significantly lower body weight and more severe limb necrosis. After operation, the blood perfusion of the operated limb of the mice in the diabetic lower extremity ulcer group and the lower extremity ischemia group decreased significantly, and on the 3rd, 7th, and 14th days after the operation, the blood perfusion in the diabetic lower extremity ulcer group and the lower extremity ischemia group gradually recovered, and on the 21st day , the lower extremity ischemia group was close to the normal level, while the diabetic lower extremity ulcer group decreased slightly. There was no limb necrosis in the diabetic group, and there was no significant change in blood perfusion. Destruction and inflammatory infiltration, the expression of CD31 was significantly increased, and SMA was significantly expressed in the diabetic lower extremity ulcer group and diabetes group, but not in the lower extremity ischemia group.

　　Conclusion The diabetic lower extremity ulcer mouse model has been successfully established. Compared with the lower extremity ischemia mouse model, the model has obvious symptoms of limb necrosis and blood perfusion recovery disorders. This model can be used to study the pathogenesis of diabetic vascular disease and therapeutic drugs. filter.