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目的观察megsin基因转染对糖尿病小鼠肾组织单核细胞趋化蛋白-1(MCP-1)及细胞间黏附分子-1(ICAM-1)表达的影响,探讨megsin在糖尿病肾病发病机制中的作用。方法制备糖尿病小鼠模型,成模后随机选取10只作为糖尿病组(B组),剩余30只每周1次经尾静脉分别注射空质粒(C组),megsin表达质粒(D组),并设立正常对照组(A组)。实验共4周,于第4周末收集各组小鼠肾组织标本,分别应用Western blot和免疫组织化学染色测定肾组织中megsin、MCP-1、ICAM-1的表达;应用电镜观察肾小球超微结构的改变。结果糖尿病小鼠肾组织megsin、MCP-1及ICAM-1表达增强,基底膜普遍增厚,系膜区基质增多,上皮细胞足突融合;megsin基因转染后上述变化趋势更加显著。结论 megsin可上调MCP-1及ICAM-1表达,促进系膜细胞增殖及系膜外基质积聚,是加速肾小球硬化的可能机制之一。
Objective To investigate the effect of megsin gene transfection on the expression of monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1) in diabetic mice and to explore the role of megsin in the pathogenesis of diabetic nephropathy effect. Methods 10 diabetic mice were randomly divided into three groups: diabetic group (group B) and blank group (group C) and megsin plasmid (group D) A normal control group (A group) was established. The experiment was performed for 4 weeks. At the end of the 4th week, the renal tissue samples from each group were collected and the expressions of megsin, MCP-1 and ICAM-1 were detected by Western blot and immunohistochemical staining respectively. Microstructure changes. Results The expression of megsin, MCP-1 and ICAM-1 in the kidney of diabetic mice increased, the basement membrane was thicker, the matrix of mesangial area was increased, the foot process of epithelial cell fusion was more obvious. The change of megsin gene was more obvious after transfection. Conclusion megsin can up-regulate the expression of MCP-1 and ICAM-1, promote mesangial cell proliferation and extra-mesangial matrix accumulation, which is one of the possible mechanisms of accelerating glomerulosclerosis.