Ohnishi H
Nihon Yakurigaku Zasshi. 1984 Feb;83(2):105-14.
The effects of intravenous administration of human or mouse pepsin were investigated on Masugi nephritis in rats and mice, which is an experimental model of glomerulonephritis in humans. Injection of anti-kidney serum to rats significantly increased the urinary protein excretion, serum levels of fibrinogen, cholesterol and immune complex, significantly decreased serum immunoglobulin G and complement levels, and caused histopathological changes such as detachment of endothelial cells from basement membrane, thickening of basement membrane, fusion of foot process and increase in hyaline cast in renal tubuli. Deposit of anti-rat IgG on glomerular capillary wall was also observed. All of these changes were ameliorated or showed a tendency to be ameliorated by intravenous administration of human pepsin, and the mechanism responsible for these effects was suggested to be selective decomposition of immune complex. Marked increase in urinary protein excretion was also observed in mice that intravenously received anti-kidney serum. This increase was suppressed by intravenous administration of human or mouse serum, the latter showing a stronger effect.
研究了静脉注射人或小鼠胃蛋白酶对大鼠和小鼠Masugi肾炎的影响,Masugi肾炎是人类肾小球肾炎的一种实验模型。给大鼠注射抗肾血清会显著增加尿蛋白排泄、纤维蛋白原、胆固醇和免疫复合物的血清水平,显著降低血清免疫球蛋白G和补体水平,并引起组织病理学变化,如内皮细胞从基底膜脱离、基底膜增厚、足突融合以及肾小管中透明管型增加。还观察到抗大鼠IgG在肾小球毛细血管壁上的沉积。静脉注射人胃蛋白酶可改善所有这些变化或显示出改善的趋势,这些作用的机制被认为是免疫复合物的选择性分解。静脉注射抗肾血清的小鼠也观察到尿蛋白排泄显著增加。静脉注射人或小鼠血清可抑制这种增加,后者显示出更强的作用。