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预处理可增强暴露于严重低压缺氧环境下的大鼠前脑线粒体抗氧化剂硫氧还蛋白-2的表达。

Preconditioning enhances the expression of mitochondrial antioxidant thioredoxin-2 in the forebrain of rats exposed to severe hypobaric hypoxia.

作者信息

Stroev Serguei A, Gluschenko Tatjana S, Tjulkova Ekaterina I, Spyrou Giannis, Rybnikova Elena A, Samoilov Michail O, Pelto-Huikko Markku

机构信息

Department of Developmental Biology, Tampere University Medical School, and Department of Pathology, Tampere University Hospital, Tampere, Finland.

出版信息

J Neurosci Res. 2004 Nov 15;78(4):563-9. doi: 10.1002/jnr.20282.

Abstract

The impact of severe hypoxia and preconditioning on the expression of the mitochondrial antioxidant thioredoxin-2 (Trx-2) in rat hippocampus (CA1, CA2, CA3 fields, and dentate gyrus) and neocortex was studied by immunocytochemistry. The preconditioning consisted of three trials of mild hypobaric hypoxia (360 Torr, 2 hr) spaced at 24 hr. The last trial was followed by severe hypobaric hypoxia (180 Torr, 3 hr) 24 hr later. Both in hippocampus and in neocortex, severe hypobaric hypoxia resulted in enhanced Trx-2 expression at 3 hr, followed by a slight decline in Trx-2 levels, which nevertheless remained increased at 24 hr elsewhere except for the CA1 region. The preconditioning considerably augmented severe hypoxia-induced Trx-2 immunoreactivity, affecting both the number of immunoreactive cells and the intensity of immunostaining. The findings suggest a role for Trx-2 in the formation of brain hypoxic/ischemic tolerance accomplished by the preconditioning.

摘要

通过免疫细胞化学方法,研究了严重缺氧及预处理对大鼠海马(CA1、CA2、CA3区和齿状回)及新皮质中线粒体抗氧化剂硫氧还蛋白-2(Trx-2)表达的影响。预处理包括三次轻度低压缺氧试验(360托,2小时),每次间隔24小时。最后一次试验24小时后进行严重低压缺氧(180托,3小时)。在海马和新皮质中,严重低压缺氧在3小时时导致Trx-2表达增强,随后Trx-2水平略有下降,不过在24小时时,除CA1区外其他部位仍保持升高。预处理显著增强了严重缺氧诱导的Trx-2免疫反应性,影响了免疫反应细胞数量及免疫染色强度。这些发现提示Trx-2在预处理所实现的脑缺氧/缺血耐受性形成中发挥作用。

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