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Induction of heme oxygenase-1 with hemin attenuates hippocampal injury in rats after acute carbon monoxide poisoning
Guan, Li; Wen, Tao; Zhang, YanLin; Wang, Xifu; Zhao, JinYuan
关键词Acute carbon monoxide poisoning Heme oxygenase Hippocampus Oxidative stress Caspase-3
刊名TOXICOLOGY
2009-08-03
DOI10.1016/j.tox.2009.06.001
262期:2页:146-152
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pharmacology & Pharmacy ; Toxicology
研究领域[WOS]Pharmacology & Pharmacy ; Toxicology
关键词[WOS]LIPID-PEROXIDATION ; OXIDATIVE STRESS ; BILIVERDIN REDUCTASE ; THERAPEUTIC TARGET ; NEURONAL DAMAGE ; UP-REGULATION ; LUNG INJURY ; BRAIN ; APOPTOSIS ; INHIBITION
英文摘要

Carbon monoxide (CO) poisoning is a major cause of brain injury and mortality; delayed neurological syndrome (DNS) is encountered in survivors of acute CO exposure. The toxic effects of CO have been attributed to oxidative stress induced by hypoxia. Heme oxygenase-1 (HO-1) is the inducible heme oxygenase isoform, and its induction acts as an important cellular defense mechanism against oxidative stress, cellular injury and disease. In this study, we examined the functional roles of HO-1 induction in a rat model of CO-exposured hippocampal injury. We report that acute CO exposure produces severe hippocampal injury in rats. However, hemin pretreatment reduced both the CO-induced rise in hippocampal water content and levels of neuronal damage in the hippocampus; survival rates at 24 h were significantly improved. Upregulation of HO-1 by hemin pretreatment resulted in a significant decrease in hippocampal levels of malondialdehyde (MDA), a marker of oxidative stress; levels of pro-apoptotic caspase-3 were also reduced. In contrast, inhibition of HO activity by administration of tin protoporphyrin IX (SnPP, a specific inhibitor of HO) abolished the neuroprotective effects of HO-1 induction. These data suggested that the upregulation of endogenous HO-1 expression therefore plays a pivotal protective role in CO neurotoxicity. Though the precise mechanisms underlying hemin-mediated HO-I induction and neuroprotection are not known, these may involve the anti-oxidant and anti-apoptotic effects of HO-1 enzyme activity. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

语种英语
WOS记录号WOS:000268941500008
项目编号200800011047 ; 30471439 ; YZZ08-2Jia-03
资助机构Doctoral Fund for New Scholars of Education of Ministry of China ; National Science Foundation Committee (NSFC) ; Seed Fund for Scientific Research of Peking University Third Hospital
引用统计
被引频次:18[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/400002259/59690
专题北京大学临床肿瘤学院_供应室
北京大学第三临床医学院_职业病科
作者单位Peking Univ, Hosp 3, Res Ctr Occupat Med, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Guan, Li,Wen, Tao,Zhang, YanLin,et al. Induction of heme oxygenase-1 with hemin attenuates hippocampal injury in rats after acute carbon monoxide poisoning[J]. TOXICOLOGY,2009,262(2):146-152.
APA Guan, Li,Wen, Tao,Zhang, YanLin,Wang, Xifu,&Zhao, JinYuan.(2009).Induction of heme oxygenase-1 with hemin attenuates hippocampal injury in rats after acute carbon monoxide poisoning.TOXICOLOGY,262(2),146-152.
MLA Guan, Li,et al."Induction of heme oxygenase-1 with hemin attenuates hippocampal injury in rats after acute carbon monoxide poisoning".TOXICOLOGY 262.2(2009):146-152.
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