动物造模,糖尿病下肢溃疡小鼠模型 z-bio 2022-11-02 308

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

　　Methods Mice were divided into three groups: lower limb ischemia group, diabetes group and diabetes lower limb ulcer group. diabetes lower limb ulcer and diabetes group were treated with intraperitoneal injection of streptozotocin (STZ) to establish type 1 diabetes model. diabetes lower limb ulcer and lower limb ischemia group were treated with high ligation of femoral artery, femoral vein and disconnection of femoral artery to establish lower limb ischemia model. diabetes group was only treated with sham operation On the 21st day, laser Doppler was used to monitor the blood flow changes and observe the limb ischemic necrosis. On the 21st day, HE slices were used to observe the histological changes and analyze the expression of platelet endothelial cell adhesion molecule-1 (PECAM ￣ 1/CD31) and anti smooth muscle antibody (SMA),

　　Results After ischemia surgery, compared with the lower limb ischemia group, the weight of the lower limb ulcer group in diabetes was significantly decreased, and the limb necrosis was more serious. After operation, the blood flow perfusion of the operating limb of mice in the diabetes lower limb ulcer group and the lower limb ischemia group decreased significantly. On the 3rd, 7th and 14th days after operation, the blood flow perfusion of the diabetes lower limb ulcer group and the lower limb ischemia group gradually recovered. On the 21st day, the lower limb ischemia group was close to the normal level, while the diabetes lower limb ulcer group slightly decreased. There was no limb necrosis in the diabetes group, and the blood flow perfusion did not change significantly, The gastrocnemius muscle tissue of the operating limb of mice in the diabetes lower limb ulcer group and the lower limb ischemia group had muscle structural destruction and inflammatory infiltration, and the expression of CD31 was significantly increased. The SMA was significantly expressed in the diabetes lower limb ulcer group and the diabetes group, but not in the lower limb ischemia group.

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