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阿尔茨海默病相关50蛋白(Alz-50)和泛素免疫反应性由猫永久性局灶性脑缺血诱导产生。

Alz-50 and ubiquitin immunoreactivity is induced by permanent focal cerebral ischaemia in the cat.

作者信息

Dewar D, Graham D I, Teasdale G M, McCulloch J

机构信息

Wellcome Surgical Institute, University of Glasgow, UK.

出版信息

Acta Neuropathol. 1993;86(6):623-9. doi: 10.1007/BF00294302.

Abstract

The effects of permanent focal cerebral ischaemia on Alz-50 and ubiquitin antibody immunohistochemical staining were investigated in vivo in the cat. Alz-50 and ubiquitin antibody staining was compared to the distribution of ischaemic cell damage. Six hours following permanent occlusion of one middle cerebral artery, Alz-50 immunoreactivity was present in neurones in the ipsilateral ischaemic cerebral cortex and caudate nucleus but not in any region of the contralateral hemisphere or in sham-operated cats. Only a proportion of neurones were stained with Alz-50 and these did not have the shrunken, pyknotic appearance characteristic of irreversible ischaemic cell damage. Ubiquitin immunoreactivity was also increased in the ischaemic hemisphere, again only a proportion of neurones were stained. The Alz-50 antibody recognises the microtubule-associated protein tau and stains neurofibrillary tangles as well as neurones vulnerable to neurofibrillary change in tissue sections of Alzheimer brain. The results indicate that there are changes in tau protein in response to an ischaemic insult, but only in some neurones, which may reflect an early stage of the degenerative process. Increased ubiquitin immunoreactivity may be a response to the presence of abnormal proteins, including tau, which are induced by an ischaemic challenge.

摘要

在猫体内研究了永久性局灶性脑缺血对Alz - 50和泛素抗体免疫组化染色的影响。将Alz - 50和泛素抗体染色与缺血性细胞损伤的分布进行比较。在一侧大脑中动脉永久性闭塞6小时后,Alz - 50免疫反应性出现在同侧缺血性大脑皮质和尾状核的神经元中,但在对侧半球的任何区域或假手术猫中均未出现。只有一部分神经元被Alz - 50染色,这些神经元没有不可逆缺血性细胞损伤特有的皱缩、固缩外观。缺血半球的泛素免疫反应性也增加,同样只有一部分神经元被染色。Alz - 50抗体识别微管相关蛋白tau,并在阿尔茨海默病脑的组织切片中对神经原纤维缠结以及易发生神经原纤维变化的神经元进行染色。结果表明,tau蛋白会因缺血性损伤而发生变化,但仅在一些神经元中,这可能反映了退行性过程的早期阶段。泛素免疫反应性增加可能是对包括tau在内的异常蛋白存在的一种反应,这些异常蛋白是由缺血性刺激诱导产生的。

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