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目的 建立弥漫性系膜增生伴局灶节段性肾小球硬化动物模型。方法 对SD大白鼠行腹部旁正中切口右肾摘除术 ,术后第 7d、30d分别尾静脉注射阿霉素 4mg/kg、3mg/kg ,第 70d制成模型。结果 该模型临床上表现为高度浮肿、大量蛋白尿、低蛋白血症、高脂血症及肾功能损害 ;病理学检查、计算机图象分析及免疫组织化学染色显示 ,肾小球主要表现为系膜基质弥漫性中至重度增生 ,系膜细胞轻度增生 ,其中约 2 2 %的肾小球出现节段性硬化 ,纤维化生长因子血小板源性生长因子 -B(PDGF -B)和成纤维细胞生长因子 -b(bFGF)的表达均增加 ,表明肾小球正处于由增生向硬化转化的过渡阶段。结论 本模型的建立为实验研究慢性肾小球疾病由系膜增生向硬化转化的机制及防治措施创造了条件。
Objective To establish an animal model of diffuse mesangial proliferation with focal segmental glomerulosclerosis. Methods Right kidneys were removed from the right middle abdominal incision of SD rats. At the 7th day and the 30th day after operation, adriamycin 4mg / kg, 3mg / kg, and 70 days were injected into the caudal vein respectively. Results The clinical manifestations of the model were high edema, massive proteinuria, hypoproteinemia, hyperlipidemia and impaired renal function. Pathological examination, computer image analysis and immunohistochemical staining showed that the glomeruli mainly manifested as Mesangial cells proliferated moderately to moderately with moderate to severe hyperplasia of the media, of which approximately 22% had glomerular segmental sclerosis. Fibroblast growth factor platelet-derived growth factor-B (PDGF-B) and fibroblasts Expression of bFGF increased, indicating that glomeruli are in the transition from hyperplasia to cirrhosis. Conclusion The establishment of this model has provided the conditions for the experimental study of the mechanism of chronic glomerular disease from mesangial proliferation to sclerotic transformation and prevention and cure measures.