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大鼠实验性自身免疫性肾小球肾炎。I. 影响诱导的因素。

Experimental autoimmune glomerulonephritis in the rat. I. Factors influencing induction.

作者信息

McCausland I P, Herdson P B, Gavin J B

出版信息

Pathology. 1976 Apr;8(2):109-15. doi: 10.3109/00313027609094436.

Abstract

Albino Holtzman, albino Wistar and hooded HS rats were injected fortnightly for 14 weeks with human glomerular basement membrane (GBM) emulsified in Freund's complete adjuvant. Half of the rats were pretreated with Freund's complete adjuvant and some were unilaterally nephrectomized. Anti-GBM antibody glomerulonephritis, characterized by proteinuria (greater than 100 mg/16 h) and a diffuse linear deposition of host immunoglobulin along the glomerular basement membrane, was first detected in Holtzman rats 4 weeks after treatment with GBM had begun, and had developed in 69% of these rats by 15 weeks. In contrast, none of the similarly treated Wistar or HS rats became proteinuric at any time, although a few showed weak glomerular fluorescence at the end of the experiment. Thus Holtzman rats are susceptible, and HS and Wistar rats are resistant to experimental anti-GBM antibody glomerulonephritis. Pretreatment with Freund's complete adjuvant apparently shortened the induction period of the experimental disease in the Holtzman rats whereas unilateral nephrectomy appeared to decrease their susceptibility to it.

摘要

将白化霍尔茨曼大鼠、白化Wistar大鼠和带帽HS大鼠每两周注射一次人肾小球基底膜(GBM),该GBM乳化于弗氏完全佐剂中,共注射14周。一半大鼠先用弗氏完全佐剂预处理,部分大鼠进行单侧肾切除。抗GBM抗体肾小球肾炎的特征为蛋白尿(大于100mg/16小时)以及宿主免疫球蛋白沿肾小球基底膜呈弥漫性线性沉积,在用GBM治疗开始4周后首次在霍尔茨曼大鼠中检测到,到15周时,69%的此类大鼠已发病。相比之下,同样接受治疗的Wistar大鼠或HS大鼠在任何时候均未出现蛋白尿,尽管少数大鼠在实验结束时显示出微弱的肾小球荧光。因此,霍尔茨曼大鼠易感,而HS大鼠和Wistar大鼠对实验性抗GBM抗体肾小球肾炎具有抗性。用弗氏完全佐剂预处理明显缩短了霍尔茨曼大鼠实验性疾病的诱导期,而单侧肾切除似乎降低了它们对该病的易感性。

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