Maternal hyperglycemia potentially inhibits the development of the fetal heart by suppressing cardiomyocyte proliferation and promoting apoptosis. Different studies have indicated that miRNAs are key regulators of cardiomyocyte proliferation, differentiation, and apoptosis and play a protective role in a variety of cardiovascular diseases. However, the biological function of miRNA-23a in hyperglycemia-related cardiomyocyte injury is not fully understood. The present study investigated the effect of miRNA-23a-3p on cell proliferation and apoptosis in a myocardial injury model induced by high glucose. H9c2 cardiomyocytes were exposed to high glucose to establish an in vitro myocardial injury model and then transfected with miRNA-23a-3p mimics. After miRNA-23a-3p transfection, lens-free microscopy was used to dynamically monitor cell numbers and confluence and calculate the cell cycle duration. CCK-8 and EdU incorporation assays were performed to detect cell proliferation. Flow cytometry was used to measured cell apoptosis. Upregulation of miRNA-23a-3p significantly alleviated high glucose-induced cell apoptosis and cell proliferation inhibition (p < 0.01 and p < 0.0001, respectively). The cell cycle of the miRNA-23a-3p mimics group was significantly shorter than that of the negative control group (p < 0.01). The expression of cell cycle–activating and apoptosis inhibition-associated factors Ccna2, Ccne1, and Bcl-2 was downregulated by high glucose and upregulated by miRNA-23a-3p overexpression in high glucose-injured H9c2 cells. miRNA-23a-3p mimics transfection before high glucose treatment had a significantly greater benefit than transfection after high glucose treatment (p < 0.0001), and the rescue effect of miRNA-23a-3p increased as the concentration increased. This study suggests that miRNA-23a-3p exerted a dose- and time-dependent protective effect on high glucose-induced H9c2 cardiomyocyte injury.

母亲高血糖可能通过抑制心肌细胞增殖和促进细胞凋亡来抑制胎儿心脏的发育。不同的研究表明，miRNAs是心肌细胞增殖、分化和凋亡的关键调节因子，在多种心血管疾病中发挥保护作用。然而，miRNA-23a 在高血糖相关心肌细胞损伤中的生物学功能尚不完全清楚。本研究调查了 miRNA-23a-3p 对高糖诱导的心肌损伤模型中细胞增殖和凋亡的影响。H9c2心肌细胞暴露于高糖条件下建立体外心肌损伤模型，然后转染miRNA-23a-3p模拟物。miRNA-23a-3p 转染后，无透镜显微镜用于动态监测细胞数量和汇合并计算细胞周期持续时间。进行 CCK-8 和 EdU 掺入测定以检测细胞增殖。流式细胞术用于测量细胞凋亡。上调 miRNA-23a-3p 显着减轻高糖诱导的细胞凋亡和细胞增殖抑制。p  < 0.01 和p  < 0.0001，分别）。miRNA-23a-3p 模拟物组的细胞周期明显短于阴性对照组（p  < 0.01）。在高糖损伤的 H9c2 细胞中，细胞周期激活和凋亡抑制相关因子Ccna2、Ccne1和Bcl-2 的表达被高糖下调，并被 miRNA-23a-3p 过表达上调。miRNA-23a-3p 模拟物在高糖处理前转染比在高糖处理后转染具有显着更大的益处（p < 0.0001)，并且随着浓度的增加，miRNA-23a-3p的拯救作用增加。该研究表明，miRNA-23a-3p 对高糖诱导的 H9c2 心肌细胞损伤具有剂量和时间依赖性保护作用。