Ogata I, Fujiwara K, Nishi T, Kuwata S, Ohta Y, Nosaka K, Oka H
First Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Am J Pathol. 1988 Jun;131(3):411-7.
Liver damage was induced in rats by a single dose of dimethylnitrosamine or D-galactosamine. In the dimethylnitrosamine model, marked glomerular IgA deposition occurred between Days 4 and 28, with its peak at Day 14. Serum IgA levels were significantly increased at Days 2 and 4, then gradually decreased, and normalized at Day 14. In the D-galactosamine model, however, no such deposition was observed, though serum IgA levels similarly increased on Days 2 and 4. IgA content in high molecular weight fraction from serum increased at Day 3 in both models. This increment remained at Day 7 only in the dimethylnitrosamine model, in which carbon clearance from the circulation was significantly decreased at Day 3. These data suggest that dysfunction of the hepatic reticuloendothelial system is a factor contributing to glomerular IgA deposition occurring in liver injury.
通过单次给予二甲基亚硝胺或D-半乳糖胺在大鼠中诱导肝损伤。在二甲基亚硝胺模型中，在第4天至28天之间出现明显的肾小球IgA沉积，在第14天达到峰值。血清IgA水平在第2天和第4天显著升高，然后逐渐下降，并在第14天恢复正常。然而，在D-半乳糖胺模型中，尽管血清IgA水平在第2天和第4天同样升高，但未观察到这种沉积。在两个模型中，血清高分子量部分的IgA含量在第3天增加。这种增加仅在二甲基亚硝胺模型中在第7天仍然存在，其中在第3天循环中的碳清除率显著降低。这些数据表明，肝网状内皮系统功能障碍是导致肝损伤中肾小球IgA沉积的一个因素。
