速冻深蚀刻法研究糖尿病大鼠肾小球基底膜超微结构。

T Moriya, S Ohno, K Nakazawa, H Shigematsu, Y Yajima
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引用次数: 9

摘要

采用速冻和深度刻蚀法观察链脲佐菌素(STZ)诱导的糖尿病大鼠肾小球基底膜(GBM)的三维超微结构。在对照组大鼠的三层GBM中,外层和内层由垂直的原纤维组成,将上皮或内皮细胞表面与中间层的网状结构连接起来。糖尿病大鼠内层弥漫性扩大,中层网状结构明显不规则,主要是由于细原纤维断裂和原纤维粘附物质增厚所致。这些超微结构变化与常规超薄切片显示的GBM的内皮下水肿、致密层状和蓬松物质相对应。提示stz诱导的糖尿病肾病的初始形态学改变是GBM中基质原纤维的破坏,似乎表明大小和/或电荷屏障的干扰。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ultrastructural study of glomerular basement membrane in diabetic rats by quick-freezing and deep-etching method.

The three-dimensional ultrastructure of glomerular basement membrane (GBM) in streptozotocin (STZ)-induced diabetic rats was examined by quick-freezing and deep-etching method. In three layers of the GBM of control rats, the outer and inner layers were formed by files of perpendicular fibrils, which connected the epithelial or endothelial cell surfaces with meshwork structures of the middle layer. In the diabetic rats, the inner layer was diffusely enlarged and the meshwork structure of the middle layer became markedly irregular due to the rupture of fine fibrils and thickening of material adherent to the fibrils. These ultrastructural changes correspond to those of subendothelial oedema, lamellation of lamina densa and fluffy material in the GBM, as revealed on conventional ultra-thin sections. It is suggested that the initial morphological change of STZ-induced diabetic nephropathy is disruption of matrix fibrils in the GBM, seemingly indicating a disturbance of size and/or charge barriers.

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