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MicroRNA-23a-3p attenuates oxidative stress injury in a mouse model of focal cerebral ischemia-reperfusion

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机构: [a]Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, 45 Changchun Street,Beijing 10O053, China [b]Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing 100053, China [c]Beijing Geriatric Medical Research Center, Beijing 1OO053, China [d]Beiing Institute for Brain Disorders, Beijing 100053, China [e]Key Laboratory of Neurodegenerativ Diseases of Ministry of Education, Beijing 10O053, China [f]Beijing Key Laboratory of Translational Medicine for Cerebrovascular Diseases, Beijing 10O0053, China
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关键词: MiR-23a-3p Cerebral ischemia Reperfusion Oxidative stress Nitric oxide

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The present study was designed to investigate the potential role of miR-23a-3p in experimental brain ischemia-reperfusion injury. Cerebral ischemia reperfusion was induced by transient middle cerebral artery occlusion (MCAO) for 1h in C57/BL6 mice. And miR-23a-3p angomir was transfected to upregulate the miR-23a-3p level. Our results showed that miR-23a-3p levels were transiently increased at 4 h after reperfusion in the pen-infarction area, while markedly increased in the infarction core at reperfusion 4 h and 24 h. Importantly, in vivo study demonstrated that miR-23a-3p angomir treatment through intracerebroventricular injection markedly decreased cerebral infarction volume after MCAO. Simultaneously, miR-23a-3p reduced peroxidative production nitric oxide (NO) and 3-nitrotyrosine (3-NT), and increased the expression of manganese superoxide dismutase (MnSOD). In vitro study demonstrated that miR-23a-3p decreased hydrogen peroxide (H2O2)-induced lactate dehydrogenase (LDH) leakage dose-dependently, and reduced protein levels of activated caspase-3 in neuro-2a cells. In addition, miR-23a-3p reduced H2O2-induced production of NO and 3-NT dose-dependently, and reversed the decreased activity of total SOD and MnSOD in neuro-2a cells. Our study indicated that miR-23a-3p suppressed oxidative stress and lessened cerebral ischemia-reperfusion injury. (C) 2014 Elsevier B.V. All rights reserved.

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出版当年[2013]版:
大类 | 3 区 医学
小类 | 4 区 神经科学
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 神经科学
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出版当年[2012]版:
Q2 NEUROSCIENCES
最新[2023]版:
Q3 NEUROSCIENCES

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第一作者机构: [a]Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, 45 Changchun Street,Beijing 10O053, China [c]Beijing Geriatric Medical Research Center, Beijing 1OO053, China [e]Key Laboratory of Neurodegenerativ Diseases of Ministry of Education, Beijing 10O053, China [f]Beijing Key Laboratory of Translational Medicine for Cerebrovascular Diseases, Beijing 10O0053, China
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通讯机构: [*1]Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing 100053, China.
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