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目的为研究人类抗肾小球基底膜肾炎(anti-glomerular basement membrane nephritis,anti-GBM)建立大鼠自身诱导的抗-GBM肾炎模型。方法健康SD大鼠40只,随机分为2组:抗-GBM肾炎模型组和正常对照组。将合成的大鼠肾小球基底膜Ⅳ型胶原α3链非胶原1区(Noncollagen Domain 1 of alpha 3 chain of typeⅣCollagen,Col4α3NC1)中的多肽序列—pCol(28-40)为抗原多肽,皮下注射免疫抗-GBM肾炎模型组;正常对照组同部位注射PBS。于第7、14、21、28、35天检测大鼠24 h尿蛋白、血肌酐及血尿素氮等生化指标变化,普通光镜观察HE,PAS染色肾组织病理改变;免疫荧光观察IgG的沉积;电镜观察肾小球基底膜,足突细胞,免疫复合物沉积的变化。结果大鼠免疫后,抗-GBM肾炎模型组在各时相点的24 h尿蛋白量、血肌酐、血尿素氮明显高于对照组(P<0.01);肾组织病理表现为肾小球内细胞数明显增多,大量细胞性新月体形成,蛋白管型多见,内皮细胞脱落、坏死;免疫荧光检查IgG沿肾小球弥漫性线样沉积;电镜观察肾小球基底膜不规则增厚,足突融合;正常对照组均未见改变。结论成功的建立了大鼠抗-GBM肾炎,该模型病变与人类抗-GBM肾炎的病变较为一致,可用于探讨抗-GBM肾炎的实验研究。
OBJECTIVE: To establish a rat model of anti-GBM nephritis induced by anti-glomerular basement membrane nephritis (anti-GBM). Methods Forty healthy SD rats were randomly divided into 2 groups: anti-GBM nephritis model group and normal control group. The polypeptide sequence -pCol (28-40) in the synthetic rat glomerular basement membrane collagen type 1 of alpha 3 chain of type IV Cololgen (Col4α3NC1) was used as antigenic polypeptide and immunized subcutaneously Anti-GBM nephritis model group; normal control group with the same site injection of PBS. On the 7th, 14th, 21st, 28th and 35th day, the urinary protein, serum creatinine, blood urea nitrogen and other biochemical indexes of 24 h were detected. The pathological changes of renal tissue were observed by light microscope. The deposition of IgG was observed by immunofluorescence Electron microscope was used to observe the changes of glomerular basement membrane, foot process cells and immune complex deposition. Results After 24 h immunization, the levels of urinary protein, serum creatinine and blood urea nitrogen in the anti-GBM nephritis model group at 24 h after immunization were significantly higher than those in the control group (P <0.01). The pathological manifestations of renal tissue were glomerular Cell number was significantly increased, a large number of cellular crescent formation, more common protein tube type, endothelial cell shedding, necrosis; IgG immunofluorescence along the glomerular diffuse linear deposition; electron microscopy of glomerular basement membrane irregular thickening , Foot process fusion; no change in the normal control group. Conclusion Rat anti-GBM nephritis has been successfully established. The pathological changes of this model are consistent with that of human anti-GBM nephritis. It can be used to investigate the anti-GBM nephritis experiment.