Decreased cpg15 augments oxidative stress in sleep deprived mouse brain
Decreased cpg15 augments oxidative stress in sleep deprived mouse brain
复制标题
cpg15 减少会增加睡眠不足小鼠大脑的氧化应激
DOI：
10.1016/j.bbrc.2019.11.132
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发表时间：
2020-02-12
影响因子：
3.1
通讯作者：
Chen, Xian-Hua
中科院分区：
文献类型：
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作者：
Li, Cheng-Jing;Li, Jun-Jie;Chen, Xian-Hua
睡眠剥夺（SD）对大脑的生理功能有不利影响。然而，根本的机制仍然难以捉摸。在本研究中，我们研究了候选可塑性相关基因15（cpg 15），神经营养基因的表达，其潜在的作用，在SD使用REM-SD小鼠模型。免疫荧光和Western blot分析显示，REM-SD 24-72 h后海马、背侧丘脑腹侧群（VENT）和大脑皮层体感区（SSP）cpg 15蛋白表达下降，而谷胱甘肽（GSH）与其氧化产物（GSSG）的比值显示，这些脑区的氧化应激水平平行增加。AAV介导的cpg 15在丘脑、海马和大脑皮层的过表达降低了这些区域的氧化应激，表明cpg 15的减少可能是导致睡眠剥夺小鼠脑中氧化应激增强的原因。总的来说，这些结果表明cpg 15可能通过抗氧化功能在SD小鼠脑中发挥保护作用。据我们所知，这是第一次提供证据表明cpg 15对SD诱导的脑氧化应激的作用。(C)2019爱思唯尔公司All rights reserved.
Sleep deprivation (SD) has detrimental effects on the physiological function of the brain. However, the underlying mechanism remains elusive. In the present study, we investigated the expression of candidate plasticity-related gene 15 (cpg15), a neurotrophic gene, and its potential role in SD using a REM-SD mouse model. Immunofluorescent and Western blot analysis revealed that the expression of cpg15 protein decreased in the hippocampus, ventral group of the dorsal thalamus (VENT), and somatosensory area of cerebral cortex (SSP) after 24-72 h of REM-SD, and the oxidative stress in these brain regions was increased in parallel, as indicated by the ratio of glutathione (GSH) to its oxidative product (GSSG). Overexpression of cpg15 in thalamus, hippocampus, and cerebral cortex mediated by AAV reduced the oxidative stress in these regions, indicating that the decrease of cpg15 might be a cause that augments oxidative stress in the sleep deprived mouse brain. Collectively, the results imply that cpg15 may play a protective function in the SD-subjected mouse brain via an anti-oxidative function. To our knowledge, this is the first time to provide evidences in the role of cpg15 against SD-induced oxidative stress in the brain. (C) 2019 Elsevier Inc. All rights reserved.