【摘要】 目的　为研究人类新月体性肾炎的发病机制 ,建立大鼠抗肾小球基底膜 (GBM)肾炎的动物模型。方法提取S -D大鼠GBM抗原 ,将此抗原免疫新西兰白兔获得抗血清 ,再将此抗血清从尾静脉一次性注射给S -D大鼠。实验分 2组 :肾炎模型组及正常对照组 ,定期于第 4天、第 14天和第 2 1天检测大鼠 2 4h尿蛋白、血肌酐及血尿素的含量和肾组织病理学改变。结果　大鼠肾炎模型组 :大鼠注射抗血清后于第 4天出现大量蛋白尿 ;第 14天血肌酐、血尿素显著升高 ,并持续上升 ;肾组织病理表现为肾小球内细胞数明显增加 ,大量新月体形成及蛋白管型 ,GBM呈不规则增厚 ,足突融合 ,内皮细胞脱落、坏死 ;免疫荧光检查见兔IgG、鼠IgG沿GBM线形分布。大鼠正常对照组以上指标均无明显改变。结论　通过动态观察大鼠抗GBM肾炎的病变变化 ,证实该模型病变与人类新月体性肾炎的病变较为一致 ,故该模型可用于探讨人类新月体性肾炎的实验研究更多还原

【Abstract】 Objective The reconstructed model of anti-GBM nephritis in rat was used to investigate the pathogenesis of human cresentic-type nephritis. Methods Anti-GBM nephritis model was established by injecting rabbit anti-rat GBM antibody (Ab) into S-D rats. All of the model rats and normal controls were studied for urinary protein, serum creatinine and serum urea on the 4th, 14th and 21th days. At the same time, the kidney specimens were collected for morphological studies. Results Rats injected with rabbit anti-GBM Ab developed heavy proteinuria on the 4th day (43.76±18.12 vs. 7.04±2.86 mg/24 h,P<0.01), and the high level of urine protein was maintained in the whole experimental period. From the 14th days, the rise of serum creatinine and urea became apparent and kept going up. Glomerular hypercellularity, crescents and protein casts were observed in the nephritis rats. Electron microscopy displayed the thickening of GBM, loss of epithelial foot processes and foci of endothelial cell detachment. Immuno-fluorescence staining revealed that rabbit IgG and rat IgG were deposited in a "linear" pattern along the GBM. Conclusion The above evidences showed that the duplication of anti-GBM nephritis model was successful.更多还原