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学科主题: 临床医学
题名:
Intense exercise can cause excessive apoptosis and synapse plasticity damage in rat hippocampus through Ca2+ overload and endoplasmic reticulum stress-induced apoptosis pathway
作者: 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
发表日期: 2014-09-20
DOI: 10.3760/cma.j.issn.0366-6999.20141191
卷: 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
所属项目编号: 30270636 ; 30671015
项目资助者: National Natural Science Foundation of China
WOS记录号: WOS:000343337300014
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/58114
Appears in Collections:北京大学第三临床医学院_运动医学研究所_期刊论文

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作者单位: Peking Univ, Hosp 3, Inst Sports Med, Beijing 100191, Peoples R China

Recommended Citation:
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.
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