TY -的A2森Aditya盟——徐Ming-Jiang AU - Cai,燕盟,瞿Aijuan盟——Shyy约翰Y.-J。文晶盟盟- Li -王,西安PY - 2017 DA - 2017/10/29 TI -即早期反应基因x - 1 (IEX-1)介导缺血性心脏保护大鼠SP - 6109061六世Preconditioning-Induced - 2017 AB -可逆心肌缺血/再灌注(I / R)或缺血预处理(IPC)与立即基因组反应;IPC-induced立即早期基因与减少梗塞大小有关。因为眼前的早期反应基因x - 1 (IEX-1)在细胞凋亡中起着核心作用,我们检查是否IEX-1施加对I / R损伤的保护作用。我们发现IEX-1 mRNA水平增加IPC-imposed鼠的心脏。然而,在I / R表达下调大鼠心脏,由原位IPC阻止。IEX-1撞倒时,IPC所强加的保护作用减弱。当地的基因传递Ad-IEX-1左心室大大降低心脏梗塞大小和改善心脏收缩功能的I / R心在老鼠。相比之下,推倒IEX-1表达式加重心肌梗塞。过度的IEX-1新生大鼠心肌细胞显著减少hypoxia-reoxygenation-induced细胞内线粒体活性氧积累和细胞凋亡。 Furthermore, IPC-induced phosphorylation and particle translocation of PKCε were impaired by knocking down IEX-1 in vivo, and overexpressing IEX-1 showed similar cardioprotection imposed by IPC. Our results demonstrate that IPC increases IEX-1 expression, which may promote phosphorylation and particle translocation of PKCε and thus reduce intracellular ROS accumulation. These beneficial effects reduce cardiomyocyte apoptosis and necrosis to alleviate cardiac infarction. SN - 1942-0900 UR - https://doi.org/10.1155/2017/6109061 DO - 10.1155/2017/6109061 JF - Oxidative Medicine and Cellular Longevity PB - Hindawi KW - ER -