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Intense exercise can cause excessive apoptosis and synapse plasticity damage in rat hippocampus through Ca2+ overload and endoplasmic reticulum stress-induced apoptosis pathway
Ding Yi; Chang Cunqing; Xie Lan; Chen Zhimin; Ai Hua
关键词Intense Exercise Exhaustion Hippocampus Endoplasmic Reticulum Stress-induced Apoptosis Synapse Plasticity Astrocytes Activation
刊名CHINESE MEDICAL JOURNAL
2014-09-20
DOI10.3760/cma.j.issn.0366-6999.20141191
127期:18页:3265-3271
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Medicine, General & Internal
研究领域[WOS]General & Internal Medicine
关键词[WOS]SYNAPTOPHYSIN ; MEMORY ; ACTIVATION ; NEURONS ; DISEASE ; DEATH
英文摘要

Background Intense exercise can cause injury and apoptosis, but few studies have reported its effect on the central nervous system (CNS). The initial reason for hippocampus injury is the excitotoxicity of glutamate and calcium overload. Intracellular free Ca2+ ([Ca2+]i) overload may trigger the apoptosis pathway and neuron damage. The aim of this study was to investigate whether intense exercise could cause hippocampus apoptosis and neuron damage and then to determine which pathway was activated by this apoptosis.

Methods We used one bout of swimming exhaustion rats as models. Intracellular ([Ca2+]i) was measured to estimate the calcium overload by Fura-2/AM immediately after exhaustion; glial fibrillary acidic protein (GFAP) and synaptophysin (SYP) immunofluorescence were performed for estimating astrocyte activation and synapse plasticity 24 hours after exhaustion. Apoptosis cells were displayed using dUTP nick end labelling (TUNEL) stain; endoplasmic reticulum (ER) stress-induced apoptosis pathway and mitochondrial apoptosis pathway were synchronously detected by Western blotting.

Results An increasing level of intracellular [Ca2+]i (P<0.01) was found in the hippocampus immediately after exhaustion. GFAP and SYP immunofluorescence showed that the astrocytes are activated, and the synapse plasticity collapsed significantly 24 hours after exhaustion. TUNEL stain showed that the number of apoptosis cells were notably raised (P<0.01); Western blotting of the apoptosis pathway showed increasing levels of caspase-3 cleavage (P<0.01), Bax (P<0.01), caspase-12 cleavage (P<0.01), C/EBP-homologous protein (CHOP) (P<0.01), and phospho-Junamino-terminal kinases (p-JNK; P<0.01) and decreasing level of Bcl-2 (P<0.01). Our results proved that exhaustion can induce hippocampus injury and apoptosis by [Ca2+]i overload, with collapsed synaptic plasticity as the injury pattern and ER stress-induced apoptosis as the activated pathway.

Conclusion Intense exercise can cause excessive apoptosis and synapse plasticity damage in the hippocampus with [Ca2+]i overload as the initial reason, and thus provides leads for therapeutic interventions in the brain health of athletes.

语种英语
WOS记录号WOS:000343337300014
项目编号30270636 ; 30671015
资助机构National Natural Science Foundation of China
引用统计
被引频次:8[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/58114
专题北京大学临床肿瘤学院_药剂科
北京大学第三临床医学院_运动医学研究所
作者单位Peking Univ, Hosp 3, Inst Sports Med, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Ding Yi,Chang Cunqing,Xie Lan,et al. Intense exercise can cause excessive apoptosis and synapse plasticity damage in rat hippocampus through Ca2+ overload and endoplasmic reticulum stress-induced apoptosis pathway[J]. CHINESE MEDICAL JOURNAL,2014,127(18):3265-3271.
APA Ding Yi,Chang Cunqing,Xie Lan,Chen Zhimin,&Ai Hua.(2014).Intense exercise can cause excessive apoptosis and synapse plasticity damage in rat hippocampus through Ca2+ overload and endoplasmic reticulum stress-induced apoptosis pathway.CHINESE MEDICAL JOURNAL,127(18),3265-3271.
MLA Ding Yi,et al."Intense exercise can cause excessive apoptosis and synapse plasticity damage in rat hippocampus through Ca2+ overload and endoplasmic reticulum stress-induced apoptosis pathway".CHINESE MEDICAL JOURNAL 127.18(2014):3265-3271.
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