机构:[a]Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, 45 Changchun Street,Beijing 10O053, China首都医科大学?脑血管病研究所首都医科大学宣武医院[b]Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing 100053, China神经内科首都医科大学宣武医院[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
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.
基金:
the National Natural Science Foundation of China(81271461,81201028,81401090,and 81471340).
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
通讯作者:
通讯机构:[*1]Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Beijing 100053, China.
推荐引用方式(GB/T 7714):
Haiping Zhao,Zhen Tao,Rongliang Wang ,et al.MicroRNA-23a-3p attenuates oxidative stress injury in a mouse model of focal cerebral ischemia-reperfusion[J].BRAIN RESEARCH.2014,1592:65-72.doi:10.1016/j.brainres.2014.09.055.
APA:
Haiping Zhao,Zhen Tao,Rongliang Wang,,Ping Liu,Feng Yan,...&Yumin Luo.(2014).MicroRNA-23a-3p attenuates oxidative stress injury in a mouse model of focal cerebral ischemia-reperfusion.BRAIN RESEARCH,1592,
MLA:
Haiping Zhao,et al."MicroRNA-23a-3p attenuates oxidative stress injury in a mouse model of focal cerebral ischemia-reperfusion".BRAIN RESEARCH 1592.(2014):65-72