Stroev Serguei A, Gluschenko Tatjana S, Tjulkova Ekaterina I, Spyrou Giannis, Rybnikova Elena A, Samoilov Michail O, Pelto-Huikko Markku
Department of Developmental Biology, Tampere University Medical School, and Department of Pathology, Tampere University Hospital, Tampere, Finland.
J Neurosci Res. 2004 Nov 15;78(4):563-9. doi: 10.1002/jnr.20282.
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.
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。