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长期链脲佐菌素诱导的糖尿病大鼠的下丘脑病变。一项半定量光镜和电镜研究。

Hypothalamic lesions in rats with long-term streptozotocin-induced diabetes mellitus. A semiquantitative light- and electron-microscopic study.

作者信息

Bestetti G, Rossi G L

出版信息

Acta Neuropathol. 1980;52(2):119-27. doi: 10.1007/BF00688009.

Abstract

Sixteen male Wistar rats, 1 year after injection of streptozotocin or vehicle, were fixed by whole-body perfusion, the brains were removed and processed for light and electron microscopy. Study of semithin sections from the hypothalamic area revealed changes in the arcuate nucleus and median eminence. The lesions, in comparison with controls, were subjected to a blind semiquantitative evaluation. The following changes were observed by light microscopy in diabetic rats: accumulation of glycogen (P < 0.01), degeneration of neurons (P < 0.05), hypotrophy of tanycytes (P < 0.01), and axonal changes. Electron microscopy of diabetic rats revealed that glycogen was increased in neuronal bodies and processes (axons, synapses), also in tanycytes, and glia cells. In neurons were seen: dilated and fragmented endoplasmic reticulum, degranulated ergastoplasm, loss of organelles, increased number of microtubuli, myelin figures, irregularities in the form of nuclei, and appearance of chromatin. The tanycytes in diabetic animals were reduced in volume, had an increased nuclear cytoplasmic ratio, a reduced number of organelles, short basal processes, and almost complete loss of the apical processes. These changes demonstrate the existence, under experimental conditions, of an encephalopathy pathogenetically related to streptozotocin-induced diabetes.

摘要

16只雄性Wistar大鼠,在注射链脲佐菌素或赋形剂1年后,通过全身灌注固定,取出大脑并进行光镜和电镜检查。对下丘脑区域半薄切片的研究揭示了弓状核和正中隆起的变化。与对照组相比,对病变进行了盲法半定量评估。通过光镜在糖尿病大鼠中观察到以下变化:糖原积累(P < 0.01)、神经元变性(P < 0.05)、伸长细胞萎缩(P < 0.01)和轴突变化。糖尿病大鼠的电镜检查显示,神经元体和突起(轴突、突触)以及伸长细胞和神经胶质细胞中的糖原增加。在神经元中可见:内质网扩张和断裂、糙面内质网脱颗粒、细胞器丢失、微管数量增加、髓鞘样结构、核形态不规则以及染色质出现。糖尿病动物的伸长细胞体积减小,核质比增加,细胞器数量减少,基底突起短,顶端突起几乎完全丧失。这些变化表明,在实验条件下存在一种与链脲佐菌素诱导的糖尿病发病机制相关的脑病。

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