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[低压缺氧暴露大鼠海马神经元中硫氧还蛋白-1的表达水平]

[Thioredoxin-1 expression level in hippocampal neurons of rats exposed to hypobaric hypoxia].

作者信息

Stroev S A, Tiul'kova E I, Glushchenko T S, Tugoĭ I A, Samoĭlov M O, Pelto-Huikko M

出版信息

Morfologiia. 2008;133(1):20-4.

PMID:19069409
Abstract

It was shown recently that preconditioning by 3-time repetitive mild hypoxia significantly augmented expression of thioredoxin-1 (Trx-1) antioxidant protein at 3 h after subsequent acute severe hypoxia in rat hippocampus as compared to the expression of this protein in non-preconditioned rats. However, it was unclear whether this augmentation was due to an accumulation of Trx-1 during the preconditioning before severe hypoxia or by a modification of reaction to severe hypoxia itself. To answer this question, Trx-1 expression level after preconditioning without subsequent severe hypoxia was studied in an experiment on 12 mature male Wistar rats. Trx-1 expression was studied by immunocytochemistry 3 h and 24 h after thrice-repeated mild hypobaric hypoxia (three 2h treatments at 360 Torr spaced by 24 h intervals). 24 h after the last hypoxic treatment, Trx-1 immunoreactivity was significantly decreased in the neurons of all the hippocampal regions studied (CA1, CA2, CA3 and dentate gyrus). In CA3 it was also decreased at 3 h after hypoxia. These findings indicate that mild preconditioning hypoxia, by itself, does not increase, but on the contrary, decreases Trx-1 expression. It may be concluded that the augmentation of Trx-1 content in the preconditioned animals is due to a modified reaction to severe hypoxia, but is not the result of Trx-1 accumulation during preconditioning.

摘要

最近的研究表明,与未进行预处理的大鼠相比,3次重复性轻度缺氧预处理可显著增强大鼠海马体在随后急性严重缺氧3小时后硫氧还蛋白-1(Trx-1)抗氧化蛋白的表达。然而,尚不清楚这种增强是由于严重缺氧前预处理期间Trx-1的积累,还是由于对严重缺氧本身反应的改变。为了回答这个问题,在一项针对12只成年雄性Wistar大鼠的实验中,研究了在没有随后严重缺氧的预处理后的Trx-1表达水平。通过免疫细胞化学方法,在三次重复的轻度低压缺氧(在360托下进行三次2小时治疗,间隔24小时)后3小时和24小时研究Trx-1表达。在最后一次缺氧治疗后24小时,在所研究的所有海马区域(CA1、CA2、CA3和齿状回)的神经元中,Trx-1免疫反应性显著降低。在CA3区,缺氧后3小时也降低。这些发现表明,轻度预处理缺氧本身不会增加,反而会降低Trx-1表达。可以得出结论,预处理动物中Trx-1含量的增加是由于对严重缺氧反应的改变,而不是预处理期间Trx-1积累的结果。

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