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Remote Ischemic Postconditioning Alleviates Cerebral Ischemic Injury by Attenuating Endoplasmic Reticulum Stress-Mediated Apoptosis

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机构: [1]Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, 45 Changchun Street, Beijing 100053, People’s Republic of China [2]Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing 100053, People’s Republic of China [3]Department of Neurosurgery, Beijing Tongren Hospital, Capital Medical University, Beijing 100073, People’s Republic of China [4]Department of Neurosurgery, Xuanwu Hospital of Capital Medical University, 45 Changchun Street, Beijing 100053, People’s Republic of China [5]Beijing Key Laboratory of Translational Medicine for Cerebrovascular Diseases, Beijing, China
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关键词: Cerebral ischemia CHOP ER stress Apoptosis Ischemic postconditioning Neuroprotection

摘要:
Remote ischemic postconditioning (RIPostC) has been proved to protect the brain from stroke, but the precise mechanism remains not fully understood. In the present study, we aimed to investigate whether RIPostC attenuates cerebral ischemia-reperfusion injury by abating endoplasmic reticulum (ER) stress response. CHOP, a multifunctional transcription factor in ER stress, regulates the expression of genes related to apoptosis, such as Bim and Bcl-2. Male SD rats were subjected to right middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion, and RIPostC was induced by three cycles of 10 min ischemia and 10 min reperfusion on bilateral femoral arteries immediately after ischemia. CHOP siRNA (CHOPi) and control siRNA (Coni) were injected into the right lateral ventricle 30 min before the beginning of ischemia. RIPostC, CHOPi, or RIPostC + CHOPi application reduced infarct volume, improved the neurological function, and decreased cell apoptosis. RIPostC increased the protein level of glucose-regulated protein 78 (GRP78) and decreased the protein level of phosphorylated-EIF2 alpha, caspase-12, and CHOP. Furthermore, the expression of CHOP, Bim and cleaved-caspase-3 was decreased, while Bcl-2 expression was increased in response to application of RIPostC, CHOPi, or RIPostC + CHOPi. In sum, RIPostC protects against ischemia-reperfusion brain injury in rats by attenuating ER stress response-induced apoptosis.

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出版当年[2013]版:
大类 | 4 区 医学
小类 | 4 区 临床神经病学 4 区 神经科学
最新[2023]版:
大类 | 2 区 医学
小类 | 2 区 临床神经病学 2 区 神经科学
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出版当年[2012]版:
Q3 CLINICAL NEUROLOGY Q3 NEUROSCIENCES
最新[2023]版:
Q1 CLINICAL NEUROLOGY Q2 NEUROSCIENCES

影响因子: 最新[2023版] 最新五年平均 出版当年[2012版] 出版当年五年平均 出版前一年[2011版] 出版后一年[2013版]

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第一作者机构: [1]Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, 45 Changchun Street, Beijing 100053, People’s Republic of China [2]Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing 100053, People’s Republic of China [5]Beijing Key Laboratory of Translational Medicine for Cerebrovascular Diseases, Beijing, China
通讯作者:
通讯机构: [1]Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, 45 Changchun Street, Beijing 100053, People’s Republic of China [2]Key Laboratory of Neurodegenerative Diseases, Ministry of Education, Beijing 100053, People’s Republic of China [4]Department of Neurosurgery, Xuanwu Hospital of Capital Medical University, 45 Changchun Street, Beijing 100053, People’s Republic of China [5]Beijing Key Laboratory of Translational Medicine for Cerebrovascular Diseases, Beijing, China
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