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Carbon monoxide offers neuroprotection from hippocampal cell damage induced by recurrent febrile seizures through the PERK-activated ER stress pathway
Han, Ying; Yi, Wenxia; Qin, Jiong; Zhao, Yang; Zhang, Jing; Chang, Xingzhi
关键词Carbon Monoxide Endoplasmic Reticulum Stress Neuronal Damage Febrile Seizure Hippocampus Perk
刊名NEUROSCIENCE LETTERS
2015-01-12
DOI10.1016/j.neulet.2014.11.040
585页:126-131
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Neurosciences
资助者National Natural Science Foundation of China ; Beijing Natural Science Foundation ; Key Clinical Project from the Ministry of Public Health ; National Key Technology R D Program ; National Natural Science Foundation of China ; Beijing Natural Science Foundation ; Key Clinical Project from the Ministry of Public Health ; National Key Technology R D Program
研究领域[WOS]Neurosciences & Neurology
关键词[WOS]ENDOPLASMIC-RETICULUM STRESS ; NITRIC-OXIDE ; NEURONAL INJURY ; PROTECTS ; APOPTOSIS ; RAT ; PATHOGENESIS ; BRAIN ; ISCHEMIA ; KINASES
英文摘要

Carbon monoxide (CO) is neuroprotective in various models of brain injury, but the precise mechanisms for this are yet to be established. In the present study, using a rat model of recurrent febrile seizures (FSs), we found an increase in plasma CO, evidence of neuronal damage and apoptosis, an increase in the expression of the endoplasmic reticulum stress (ERS) marker glucose-regulated protein 78 (GRP78) and C/EBP homologous binding protein (CHOP), and an increase in phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (p-PERK)/eukaryotic translation initiation factor 2 alpha (p-eIF2 alpha) in the hippocampus after 10 FSs. Administration of Hemin (a CO donor) in FS rats alleviated the neuronal damage, reduced neuronal apoptosis, upregulated GRP78 expression, decreased CHOP, and increased p-PERK and p-eIF2 alpha expression in the hippocampus, compared to FS control rats. In contrast, treating FS rats with ZnPP-IX (a CO synthase inhibitor) aggravated the neuronal damage, enhanced neuronal apoptosis, downregulated GRP78 expression, increased CHOP, and decreased p-PERK and p-eIF2 alpha expression, compared to FS control rats. These results suggest that endogenous CO limits the neuronal damage induced by recurrent FSs, through the PERK-activated ERS pathway. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

语种英语
所属项目编号81200998 ; 7092105 ; 7112131 ; 2012BAI03B02
资助者National Natural Science Foundation of China ; Beijing Natural Science Foundation ; Key Clinical Project from the Ministry of Public Health ; National Key Technology R D Program ; National Natural Science Foundation of China ; Beijing Natural Science Foundation ; Key Clinical Project from the Ministry of Public Health ; National Key Technology R D Program
WOS记录号WOS:000349194400025
引用统计
被引频次:9[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/400002259/56237
专题北京大学第一临床医学院_儿科
作者单位Peking Univ, Hosp 1, Dept Pediat, Beijing, Peoples R China
推荐引用方式
GB/T 7714
Han, Ying,Yi, Wenxia,Qin, Jiong,et al. Carbon monoxide offers neuroprotection from hippocampal cell damage induced by recurrent febrile seizures through the PERK-activated ER stress pathway[J]. NEUROSCIENCE LETTERS,2015,585:126-131.
APA Han, Ying,Yi, Wenxia,Qin, Jiong,Zhao, Yang,Zhang, Jing,&Chang, Xingzhi.(2015).Carbon monoxide offers neuroprotection from hippocampal cell damage induced by recurrent febrile seizures through the PERK-activated ER stress pathway.NEUROSCIENCE LETTERS,585,126-131.
MLA Han, Ying,et al."Carbon monoxide offers neuroprotection from hippocampal cell damage induced by recurrent febrile seizures through the PERK-activated ER stress pathway".NEUROSCIENCE LETTERS 585(2015):126-131.
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