NDUFA4L2 protects against ischaemia/reperfusion-induced cardiomyocyte apoptosis and mitochondrial dysfunction by inhibiting complex I.
作者： Jianhua Li , Caiyan Bai , Junxia Guo , Wanqian Liang , Jingning Long
关键词: Molecular biology 、 MPTP 、 Western blot 、 Protein subunit 、 Flow cytometry 、 Apoptosis 、 Cytochrome c 、 Mitochondrion 、 Biology 、 Gene silencing
摘要: Myocardial ischaemia/reperfusion (I/R) injury may cause the apoptosis of cardiomyocytes as well mitochondrial dysfunction. The aims present study were to investigate whether NADH dehydrogenase 1 alpha subcomplex subunit 4-like 2 (NDUFA4L2) on myocardial ischaemia-reperfusion and underlying molecular mechanism. hypoxia-reperfusion (H/R) model was established in vitro using H9c2 cells simulate I/R injury. NDUFA4L2 complex I expression levels detected RT-PCR western blot. evaluated by flow cytometry Bax Bcl-2 function assessed ATP concentration, mPTP opening cytochrome c (cyto C) expression. Our data indicated that significantly down-regulated H/R Overexpression led a dramatic prevention H/R-induced accompanied decrease an increase Bcl-2. Meanwhile, augmentation dramatically prevented dysfunction caused reflecting increased delayed opening, cyto C Moreover, activation heightened negatively regulated NDUFA4L2. Silencing conspicuously attenuated cell Taken together, our findings demonstrated protects against preventing myocardium via I, be potential therapeutic approach for attenuating
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