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学科主题: 基础医学
题名:
17 beta-Estradiol prevents cell death and mitochondrial dysfunction by an estrogen receptor-dependent mechanism in astrocytes after oxygen-glucose deprivation/reperfusion
作者: Guo, Jiabin1,2,4; Duckles, Sue P.2; Weiss, John H.3; Li, Xuejun1; Krause, Diana N.2
关键词: Estrogen ; Protection ; Astrocyte ; Ischemic injury ; Mitochondria ; Free radicals
刊名: FREE RADICAL BIOLOGY AND MEDICINE
发表日期: 2012-06-01
DOI: 10.1016/j.freeradbiomed.2012.03.005
卷: 52, 期:11-12, 页:2151-2160
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Endocrinology & Metabolism
研究领域[WOS]: Biochemistry & Molecular Biology ; Endocrinology & Metabolism
关键词[WOS]: ESTRADIOL-MEDIATED PROTECTION ; INTRACELLULAR CALCIUM-RELEASE ; IN-VITRO ; PROGESTERONE SYNTHESIS ; ISCHEMIC-INJURY ; EXPLANT CULTURES ; OXIDATIVE STRESS ; BRAIN-INJURY ; BETA ; NEUROPROTECTION
英文摘要:

17 beta-Estradiol (E2) has been shown to protect against ischemic brain injury, yet its targets and the mechanisms are unclear. E2 may exert multiple regulatory actions on astrocytes that may greatly contribute to its ability to protect the brain. Mitochondria are recognized as playing central roles in the development of injury during ischemia. Increasing evidence indicates that mitochondrial mechanisms are critically involved in E2-mediated protection. In this study, the effects of E2 and the role of mitochondria were evaluated in primary cultures of astrocytes subjected to an ischemia-like condition of oxygen-glucose deprivation (OGD)/reperfusion. We showed that E2 treatment significantly protects against OGD/reperfusion-induced cell death as determined by cell viability, apoptosis, and lactate dehydrogenase leakage. The protective effects of E2 on astrocytic survival were blocked by an estrogen receptor (ER) antagonist (ICI-182,780) and were mimicked by an ER alpha agonist selective for ER a (PPT), but not by an ER agonist selective for ER beta (DPN). OGD/reperfusion provoked mitochondrial dysfunction as manifested by an increase in cellular reactive oxygen species production, loss of mitochondrial membrane potential, and depletion of ATP. E2 pretreatment significantly inhibited OGD/reperfusion-induced mitochondrial dysfunction, and this effect was also blocked by ICI-182,780. Therefore, we conclude that E2 provides direct protection to astrocytes from ischemic injury by an ER-dependent mechanism, highlighting an important role for ER alpha. Estrogen protects against mitochondrial dysfunction at the early phase of ischemic injury. However, overall implications for protection against brain ischemia and its complex sequelae await further exploration. (C) 2012 Elsevier Inc. All rights reserved.

语种: 英语
所属项目编号: R01 HL-50775 ; 81102424 ; 81020108031 ; 31079630 ; 30973558 ; 20073020
项目资助者: U.S. National Heart, Lung, and Blood Institute ; National Natural Science Foundation of China ; China Scholarship Council
WOS记录号: WOS:000305857300001
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/50709
Appears in Collections:基础医学院_药理学系_期刊论文

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作者单位: 1.Peking Univ, Sch Basic Med, Dept Pharmacol, State Key Lab Nat Biomimet Drugs, Beijing 100191, Peoples R China
2.Univ Calif Irvine, Sch Med, Dept Pharmacol, Irvine, CA 92697 USA
3.Univ Calif Irvine, Sch Med, Dept Neurol, Irvine, CA 92697 USA
4.Acad Mil Med Sci, Inst Dis Control & Prevent, Evaluat & Res Ctr Toxicol, Beijing 100071, Peoples R China

Recommended Citation:
Guo, Jiabin,Duckles, Sue P.,Weiss, John H.,et al. 17 beta-Estradiol prevents cell death and mitochondrial dysfunction by an estrogen receptor-dependent mechanism in astrocytes after oxygen-glucose deprivation/reperfusion[J]. FREE RADICAL BIOLOGY AND MEDICINE,2012,52(11-12):2151-2160.
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