糖尿病下肢溃疡小鼠模型 z-bo 2020-12-09 343

　　Objective 　 To establish and evaluate a mouse model of diabetic lower extremity ulcers, reveal the changes in blood flow and pathophysiology of the surgical limbs of diabetic lower extremity ulcers in mice, and explore the pathogenesis of diabetic lower extremity ulcers to provide a basis and reference for studying 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 intraperitoneally injected with streptozotocin (STZ) to establish type 1 diabetes model. Diabetic lower extremity ulcer and lower extremity ischemia group were used The lower limb ischemia model was established by ligating the femoral artery and vein at a high position and severing the femoral artery. The diabetes group was treated with sham operation only, and the blood flow was monitored by laser Doppler on the 0th, 3rd, 7th, 14th and 21st days after the operation. Change, observe the avascular necrosis of the limbs, observe the tissue morphology changes after the 21st day, and analyze the expression of platelet-endothelial cell adhesion molecule-1 (PECAM-1/CD31) and anti-smooth muscle antibody (SMA).

　　Results 　 After ischemia, compared with the lower limb ischemia group, the weight of the diabetic lower limb ulcer group decreased significantly and the limb necrosis was more serious. After the operation, the blood perfusion of the surgical limb of the mice in the diabetic lower limb ulcer group and the lower limb ischemia group decreased significantly. On the 3rd, 7th, and 14th day after the operation, the blood perfusion of the diabetic lower limb ulcer group and the lower limb 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 obvious change in blood perfusion. The gastrocnemius muscle of the operating limb of the diabetic lower extremity ulcer group and the lower extremity ischemia group had muscle structure Damage and inflammatory infiltration, the expression of CD31 was significantly increased, the expression of SMA was significant in the diabetic lower limb ulcer group and the diabetic group, but the expression in the lower limb ischemia group was not obvious. Conclusion A mouse model of diabetic lower extremity ulcer was successfully established. Compared with a mouse model of lower extremity ischemia, this model has obvious symptoms of limb necrosis and impaired blood perfusion recovery. This model can be used to study the pathogenesis of diabetic vascular disease and therapeutic drugs Of screening.