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中度低压缺氧大鼠海马神经元中硫氧还蛋白-1的表达水平

Thioredoxin-1 expression levels in rat hippocampal neurons in moderate hypobaric hypoxia.

作者信息

Stroev S A, Tyul'kova E I, Glushchenko T S, Tugoi I A, Samoilov M O, Pelto-Huikko M

机构信息

Department of Developmental Biology, University Medical School, Tampere, Finland.

出版信息

Neurosci Behav Physiol. 2009 Jan;39(1):1-5. doi: 10.1007/s11055-008-9091-5. Epub 2008 Dec 17.

Abstract

Previous studies have demonstrated that preconditioning (PC) with three sessions of moderate hypoxia significantly increases the expression of the antioxidant protein thioredoxin-1 (Trx-1) in the rat hippocampus by 3 h after subsequent acute severe hypoxia as compared with non-preconditioned animals. However, it remained unclear whether this increase in Trx-1 accumulation during PC is induced before severe hypoxia or is a modification of the response to severe hypoxia. This question was addressed in the present investigation using experiments on 12 adult male Wistar rats with studies of Trx-1 expression after PC without subsequent severe hypoxia. Immunocytochemical studies were performed 3 and 24 h after three episodes of moderate hypobaric hypoxia (three sessions of 2 h at 360 mmHg with 24-h intervals). Immunoreactivity to Trx-1 24 h after the last session was significantly decreased in neurons in all the areas of the hippocampus studied (CA1, CA2, CA3, and the dentate gyrus). Immunoreactivity in CA3 was also decreased 3 h after hypoxia. These results provide evidence that moderate preconditioning hypoxia itself not only does not increase, but even significantly decreases Trx-1 expression. Thus, increases in Trx-1 contents in the hippocampus of preconditioned animals after severe hypoxia are not associated with the accumulation of this protein during PC, but with a PC-induced modification of the reaction to severe hypoxia.

摘要

先前的研究表明,与未进行预处理的动物相比,经过三次中度缺氧预处理(PC)的大鼠在随后急性严重缺氧3小时后,海马体中抗氧化蛋白硫氧还蛋白-1(Trx-1)的表达显著增加。然而,PC过程中Trx-1积累的增加是在严重缺氧之前诱导的,还是对严重缺氧反应的一种改变,仍不清楚。本研究通过对12只成年雄性Wistar大鼠进行实验,并研究PC后无后续严重缺氧情况下Trx-1的表达,来解决这个问题。在三次中度低压缺氧发作(在360 mmHg下进行三次2小时的 sessions,间隔24小时)后3小时和24小时进行免疫细胞化学研究。在最后一次sessions后24小时,在所研究的海马体所有区域(CA1、CA2、CA3和齿状回)的神经元中,对Trx-1的免疫反应性显著降低。缺氧后3小时,CA3中的免疫反应性也降低。这些结果证明,中度预处理缺氧本身不仅不会增加,甚至会显著降低Trx-1的表达。因此,预处理动物在严重缺氧后海马体中Trx-1含量的增加与PC期间该蛋白的积累无关,而是与PC诱导的对严重缺氧反应的改变有关。

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