Long-term electromagnetic pulse exposure induces Abeta deposition and cognitive dysfunction through oxidative stress and overexpression of APP and BACE1
Long-term electromagnetic pulse exposure induces Abeta deposition and cognitive dysfunction through oxidative stress and overexpression of APP and BACE1
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长期电磁脉冲暴露通过氧化应激和 APP 和 BACE1 过度表达诱导 Abeta 沉积和认知功能障碍
DOI：
10.1016/j.brainres.2016.02.053
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发表时间：
2016-07-01
期刊：
影响因子：
2.9
通讯作者：
Guo, Guo-Zhen
中科院分区：
文献类型：
--
作者：
Jiang, Da-Peng;Li, Jin-hui;Guo, Guo-Zhen
近年来，电磁场（EMF）对阿尔茨海默病（AD）的有害或有益影响的文献逐渐增多。本研究旨在探讨电磁脉冲（EMP）暴露与大鼠AD发生的关系及其机制，重点探讨氧化应激（OS）在其中的作用。健康雄性SD大鼠55只，连续染毒8个月。采用Morris水迷宫（MWM）测试大鼠的认知和记忆能力。以超氧化物歧化酶（SOD）活性和谷胱甘肽（GSH）含量为指标检测OS水平。我们发现，长期电磁脉冲暴露诱导大鼠认知功能损害。长期电磁脉冲照射后海马组织β-淀粉样蛋白（A β）含量增加。检测海马神经元OS。Western blotting和免疫组化结果显示，EMP暴露组大鼠海马A β蛋白及其寡聚体含量均高于假暴露组。EMP暴露组大鼠海马组织β位点App裂解酶（BACE 1）和微管相关蛋白1轻链3-II（LC 3-II）的含量也明显高于假暴露组。EMP染毒组SOD活性和GSH含量低于假染毒组（p < 0.05）。EMP暴露诱导OS的机制包括淀粉样前体蛋白（APP）异常裂解增加。虽然还需要进一步的研究，目前的结果表明，长期暴露于电磁脉冲对大鼠的认知能力有害，并可能导致AD样病理表现。(C)© 2016 Elsevier B. V.版权所有。
A progressively expanded literature has been devoted in the past years to the noxious or beneficial effects of electromagnetic field (EMF) to Alzheimer's disease (AD). This study concerns the relationship between electromagnetic pulse (EMP) exposure and the occurrence of AD in rats and the underlying mechanisms, focusing on the role of oxidative stress (OS). 55 healthy male Sprague Dawley (SD) rats were used and received continuous exposure for 8 months. Morris water maze (MWM) test was conducted to test the ability of cognitive and memory. The level of OS was detected by superoxide dismutase (SOD) activity and glutathione (GSH) content. We found that long-term EMP exposure induced cognitive damage in rats. The content of beta-amyloid (A beta) protein in hippocampus was increased after long-term EMP exposure. OS of hippocampal neuron was detected. Western blotting and immunohistochemistry (IHC) assay showed that the content of A beta protein and its oligomers in EMP-exposed rats were higher than that of sham-exposed rats. The content of Beta Site App Cleaving Enzyme (BACE1) and microtubule-associated protein 1 light chain 3-II (LC3-II) in EMP-exposed rats hippocampus were also higher than that of sham-exposed rats. SOD activity and GSH content in EMP-exposed rats were lower than sham-exposed rats (p < 0.05). Several mechanisms were proposed based on EMP exposure induced OS, including increased amyloid precursor protein (APP) aberrant cleavage. Although further study is needed, the present results suggest that long-term EMP exposure is harmful to cognitive ability in rats and could induce AD-like pathological manifestation. (C) 2016 Elsevier B.V. All rights reserved.