动物造模,糖尿病下肢溃疡小鼠模型 z-bio 2021-04-19 266

　　Purpose: To establish and evaluate a mouse model of diabetic leg ulcers, to clarify the blood flow of diabetic leg ulcers in mice and the pathophysiological changes of surgical limbs, to study its etiology, to lay the foundation for diabetes research, and to provide support for peripheral vascular diseases According to reference.

　　Method: The mice were divided into lower limb ischemia group, diabetes group, diabetic calf ulcer group, diabetic calf ulcer and diabetes group, intraperitoneal injection of streptozotocin (STZ) to establish an ischemic group. The lower limb ischemia model was established by ligating the femoral artery and vein at a high position and cutting off the femoral artery. Diabetes group received only sham surgery treatment, and used laser Doppler monitoring on the 0th, 3rd, 7th and 14th days. Observe changes in blood flow, without vascular necrosis of the limbs, 21 days later, HE slices to observe histological changes, platelet-endothelial cell adhesion molecule 1 (PECAM-1/CD31) and anti-smooth muscle antibody (SMA)),

　　Result: After the missing bleeding operation, compared with the lower limb ischemia group, the weight of the diabetic lower limb ulcer group was significantly reduced, and the limb necrosis was more serious. After the operation, the blood perfusion of the surgical limb of the mice in the diabetic calf ulcer group and the lower limb ischemia group was significantly reduced. On the 3rd, 7th and 14th day after the operation, the blood perfusion of the diabetic lower limbs was significantly reduced. The limb ulcer group and the lower limb ischemia group gradually recovered. On the 21st day, the lower limb ischemia group reached the normal level, but the diabetic calf ulcer group decreased slightly. There was no limb necrosis in the diabetes group. The gastrostomy muscle tissue of the surgical limb in the diabetic calf ulcer group and the lower limb ischemia group had muscle structural damage and inflammatory infiltration. The expression of CD31 in diabetic patients was significantly increased, and the expression of SMA was significantly increased in the calf ulcer group and diabetes Group, but its occurrence in the lower limb ischemia group is still unclear.

　　Conclusion: We have successfully established a mouse model of diabetic leg ulcers. Compared with the mouse model of lower limb ischemia, this model has obvious symptoms of lower limb necrosis and impaired hemoperfusion recovery. This model is used for diabetic vascular disease and therapeutic drug screening.