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低压缺氧后处理的神经保护作用伴随着大鼠海马区DNA保护和脂质过氧化的变化。

Neuroprotective effect of hypobaric hypoxic postconditioning is accompanied by dna protection and lipid peroxidation changes in rat hippocampus.

作者信息

Vetrovoy Oleg, Tulkova Ekaterina, Sarieva Ksenia, Kotryahova Elena, Zenko Mikhail, Rybnikova Elena

机构信息

Laboratory of Regulation of Brain Neuronal Functions, Pavlov Institute of Physiology, Russian Academy of Sciences, Makarova emb. 6, 199034 Saint-Petersburg, Russian Federation; Department of Biochemistry, Faculty of Biology, Saint-Petersburg State University, Universitetskaya emb. 7-9, 199034 Saint- Petersburg, Russian Federation.

Laboratory of Regulation of Brain Neuronal Functions, Pavlov Institute of Physiology, Russian Academy of Sciences, Makarova emb. 6, 199034 Saint-Petersburg, Russian Federation.

出版信息

Neurosci Lett. 2017 Feb 3;639:49-52. doi: 10.1016/j.neulet.2016.12.054. Epub 2016 Dec 23.

DOI:10.1016/j.neulet.2016.12.054
PMID:28025115
Abstract

The present study was performed to explore the effect of severe hypobaric hypoxia (180Torr, 3h) and severe hypoxia followed by hypoxic postconditioning (360Torr, 2h, 3 episodes) on DNA fragmentation and dynamics of lipid peroxidation products in rat hippocampus. The severe hypoxia induced intense DNA fragmentation in the hippocampus. A persistent decrease of thiobarbituric acid reactive substances in the hippocampus was also detected in response to severe hypoxia while the levels of Schiff bases did not significantly change. The postconditioning prevented severe hypoxia-induced DNA fragmentation, returned the levels of thiobarbituric acid reactive substances to the baseline and decreased the levels of Schiff bases. These findings indicate that the neuroprotective effect of hypoxic postconditioning on hippocampal neurons detected as suppression of hypoxia-induced DNA fragmentation is accompanied by the changes in lipid peroxidation processes.

摘要

本研究旨在探讨严重低压缺氧(180托,3小时)以及严重缺氧后进行缺氧后处理(360托,2小时,3次)对大鼠海马体中DNA片段化及脂质过氧化产物动态变化的影响。严重缺氧诱导海马体中出现强烈的DNA片段化。同时还检测到,作为对严重缺氧的反应,海马体中硫代巴比妥酸反应性物质持续减少,而席夫碱水平未发生显著变化。后处理可预防严重缺氧诱导的DNA片段化,使硫代巴比妥酸反应性物质水平恢复至基线,并降低席夫碱水平。这些发现表明,缺氧后处理对海马神经元的神经保护作用表现为抑制缺氧诱导的DNA片段化,同时伴有脂质过氧化过程的变化。

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