Myocardial ischemia/reperfusion (I/R) injury is a clinically fatal disease, caused by restoring myocardial blood supply after a period of ischemia or hypoxia. However, the underlying mechanism remains unclear. Recently, increasing evidence reveal that microRNAs (miRs) participate in myocardial I/R injury. This study aimed to investigate whether miR-128-1-5p contributed to cardiomyocyte apoptosis induced by myocardial I/R injury. Here, we showed that the expression of miR-128-1-5p was decreased in mice following myocardial I/R injury. Down-regulation of miR-128-1-5p was also showed in H9c2 cardiomyocytes after hypoxia/reoxygenation (H/R), and in neonatal rat cardiomyocytes (NRCMs) with H₂O₂ treatment. Importantly, we found that overexpression of miR-128-1-5p ameliorates cardiomyocyte apoptosis both in H9c2 cardiomyocytes and NRCMs. Moreover, we also found that growth arrest DNA damage-inducible gene 45 gamma (Gadd45g) is identified as a direct target of miR-128-1-5p, which negatively regulated Gadd45g expression. Additionally, silencing of Gadd45g inhibits cardiomyocyte apoptosis in H9c2 cardiomyocytes and NRCMs. These results reveal a novel mechanism by which miR-128-1-5p regulates Gadd45g-mediated cardiomyocyte apoptosis in myocardial I/R injury.

心肌缺血/再灌注（I / R）损伤是一种临床致命疾病，由缺血或缺氧一段时间后恢复心肌供血引起。但是，其潜在机制仍不清楚。最近，越来越多的证据表明microRNA（miR）参与了心肌I / R损伤。本研究旨在探讨miR-128-1-5p是否有助于心肌I / R损伤诱导的心肌细胞凋亡。在这里，我们显示了心肌I / R损伤后miR-128-1-5p的表达降低了。在缺氧/复氧（H / R）后的H9c2心肌细胞中以及在H ₂ O ₂新生的大鼠心肌细胞（NRCM）中也显示出miR-128-1-5p的下调。治疗。重要的是，我们发现miR-128-1-5p的过表达改善了H9c2心肌细胞和NRCM中的心肌细胞凋亡。此外，我们还发现生长停滞DNA损伤诱导基因45γ（Gadd45g）被确定为miR-128-1-5p的直接靶点，而miR-128-1-5p负调控了Gadd45g的表达。此外，沉默Gadd45g可抑制H9c2心肌细胞和NRCM中的心肌细胞凋亡。这些结果揭示了miR-128-1-5p调节心肌I / R损伤中Gadd45g介导的心肌细胞凋亡的新机制。