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作 者:刘洁[1] 李英[2] 刘茂东[2] 刘莉[3] 孟杰[4] 马永军 杨惠
机构地区:[1]河北大学附属医院内分泌科,保定071000 [2]河北医科大学第三医院肾内科,石家庄050051 [3]保定市第一医院儿科,071000 [4]河北大学附属医院消化科,保定071000 [5]满城县医院肿瘤内分泌科,072150
出 处:《免疫学杂志》2012年第9期755-758,763,共5页Immunological Journal
基 金:河北省自然科学基金资助项目(C2010000583)
摘 要: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。To observe the effects of megsin gene transfection on the expression of monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1), and investigate the role of megsin in the pathogenesis of diabetic nephropathy, we established a model of diabetic mouse. Randomly selected 10 mice as the diabetic group (group B). The remaining 30 mice were respectively injected pCMV-SPORT6.1 (group C), Megsin- pCMV.SPORT6.1 (group D) via tail vein once a week, and the normal control group was established (group A). All animals were sacrificed at week 4 and kidney tissues were harvested. The expression levels of megsin, MCP-1, and ICAM-1 were detected by immunohistochemistry and Western blot. Electron microscopy was used to observe the pathological changes. In diabetic mouse kidney, we observed the increased expression of megsin, MCP-1, and ICAM-1, irregular thickening of glomerular basement membrane, mesangial expansion, and fusion of foot processes. The above changes were more significant after megsin gene transfection. Our results suggested that megsin gene can up-regulate the expression of MCP-1 and ICAM-1, induce mesangial cell proliferation and mesangial extracellular matrix accumulation, which is probably one of the mechanisms of accelerating glomerulosclerosis.
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