MicroRNAs (miRNAs) are recognized to hold essential parts in the course of pathophysiology participating in myocardial ischemia/reperfusion (I/R) injury. The current study was intended to appraise the functional implication and underlying regulatory mechanism action of miR-20a in myocardial I/R injury. In cardiomyocyte hypoxia/reoxygenation (H/R) model simulating I/R, we observed that miR-20a was diminished in H9c2 cells subjected to H/R. The miR-20a mimics promoted cardiomyocyte viability and reduced H/R-triggered cell apoptosis, while the miR-20a inhibitors induced the inverse response in H9c2 cells subjected to H/R injury. Moreover, we ascertained that TLR4 was one downstream target gene of miR-20a and revealed that miR-20a might hold its protective action on cardiomyocytes subjected to H/R by inactivating p38 MAPK/JNK signaling. In summary, this study highlighted the relieved potential of miR-20a against cardiomyocyte H/R injury and suggested its favorable therapeutic role for myocardial I/R injury.

中文翻译：

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miR-20a通过靶向TLR4和抑制p38 MAPK / JNK信号传导对缺氧/复氧治疗对心肌细胞活力和细胞凋亡的保护作用。

MicroRNA（miRNA）被认为在参与心肌缺血/再灌注（I / R）损伤的病理生理学过程中具有重要组成部分。本研究旨在评估miR-20a在心肌I / R损伤中的功能含义和潜在的调控机制作用。在模拟I / R的心肌细胞缺氧/复氧（H / R）模型中，我们观察到在经受H / R的H9c2细胞中miR-20a减少了。miR-20a模拟物可促进心肌细胞活力并减少H / R触发的细胞凋亡，而miR-20a抑制剂可在遭受H / R损伤的H9c2细胞中诱导逆反应。此外，我们确定TLR4是miR-20a的一个下游靶基因，并揭示了miR-20a可能通过灭活p38 MAPK / JNK信号传导而对经受H / R的心肌细胞保持其保护作用。综上所述，