Hirszel P, Michaelson J H, Dodge K, Yamase H, Bigazzi P E
Surv Synth Pathol Res. 1985;4(5-6):412-22.
The repeated administration of mercuric chloride to BN rats induces the production of anti-GBM. In the present paper, we describe the immunohistopathology and histopathology of the kidneys from mercuricchloride-treated rats. Direct immunofluorescence demonstrated bright linear deposits of immunoglobulins at the level of the GBM of the kidney. Light microscopy failed to reveal substantial glomerular changes, but electron microscopy demonstrated a spectrum of ultrastructural alterations of the glomeruli (including the detachment of endothelial cells from the GBM and the presence of electron-opaque deposits). In the aggregate, these findings are suggestive of membranous glomerulonephritis. We also investigated whether treatment with low doses of PG had any effect on the course of this experimental model of autoimmune renal disease. Two groups of mercuric-chloride-treated BN rats received different doses of DMPGE2. This resulted in significantly lower levels of circulating autoantibodies to the GBM, as well as a decrease in the amounts of rat immunoglobulins bound to the kidneys and an increase in proteinuria. On the other hand, there were no major differences in renal histopathology between rats treated with DMPGE2 and controls.
向BN大鼠反复注射氯化汞会诱导抗肾小球基底膜（GBM）的产生。在本文中，我们描述了氯化汞处理大鼠肾脏的免疫组织病理学和组织病理学情况。直接免疫荧光显示在肾脏GBM水平有明亮的免疫球蛋白线性沉积。光学显微镜未能发现明显的肾小球变化，但电子显微镜显示肾小球存在一系列超微结构改变（包括内皮细胞与GBM分离以及电子致密沉积物的存在）。总体而言，这些发现提示为膜性肾小球肾炎。我们还研究了低剂量前列腺素（PG）治疗对这种自身免疫性肾脏疾病实验模型病程是否有任何影响。两组氯化汞处理的BN大鼠接受了不同剂量的二甲基前列腺素E2（DMPGE2）。这导致循环中抗GBM自身抗体水平显著降低，以及与肾脏结合的大鼠免疫球蛋白量减少和蛋白尿增加。另一方面，用DMPGE2处理的大鼠与对照组在肾脏组织病理学上没有重大差异。
