论文部分内容阅读
雄性Wistar大鼠,除预留空白组大鼠外,其余动物通过饲喂高糖高脂饲料4周并腹腔注射30 mg·kg-1链脲佐菌素(STZ)造成2型糖尿病模型后,按血糖均衡分组并给予相应药物治疗8周,8周末于大鼠背部做直径2 cm圆形切口。继续给药10 d,期间每2 d测量创面面积,10 d后剪下创面肉芽组织用于病理学检查及血管内皮生长因子(VEGF)、磷脂酰肌醇-3激酶(PI3K)、磷酸化的胞外调节蛋白激酶(p-ERK)蛋白在创面组织的表达情况。结果显示,与模型组相比,芪蛭降糖胶囊(2.24g·kg-1)皮肤创面面积在创面形成第6天和第10天明显减小;溃疡面炎症反应明显减轻;芪蛭降糖胶囊能提高糖尿病大鼠皮肤创面组织中VEGF蛋白表达,抑制ERK的磷酸化,提示芪蛭降糖胶囊可以促进糖尿病皮肤溃疡的愈合,其机制可能与调节VEGF和p-ERK蛋白的表达有关。
In the male Wistar rats, except the rats in the blank group, the other animals were given type 2 diabetes mellitus by feeding high glucose and high fat diet for 4 weeks and intraperitoneally injecting streptozotocin 30 mg · kg -1 (STZ) Divided by glycemic control and given the appropriate drug treatment for 8 weeks, 8 weeks in the back of the rat made 2 cm in diameter circular incision. The rats were sacrificed every 10 days, and the wound area was measured every 2 days. After 10 days, the wound granulation tissue was excised for pathological examination and VEGF, PI3K, phosphorylation Expression of extracellular regulated protein kinase (p-ERK) protein in wound tissues. The results showed that compared with the model group, the skin wound area of QZHG capsule (2.24g · kg-1) decreased significantly on the 6th day and the 10th day after wound formation; the inflammatory response in the ulcer surface was significantly reduced; Capsule can improve the expression of VEGF protein and inhibit the phosphorylation of ERK in the wound tissue of diabetic rats, suggesting that QHD can promote the healing of diabetic skin ulcers. The mechanism may be related to the regulation of VEGF and p-ERK protein expression.