This study aimed to investigate the effect and mechanism of miR-26a-5p on cardiomyocyte injury induced by hypoxia/reoxygenation (H/R).

After construction of an H/R model in rat cardiomyocyte H9c2 cells, miR-26a-5p in the cells was interfered with (cells transfected with miR-26a-5p inhibitor) or overexpressed (cells transfected with a miR-26a-5p mimics). The viability and the apoptosis rate of cells in each group were detected using CCK-8 and flow cytometry; the relationship between miR-26a-5p and WNT5A was verified by a dual-luciferase reporter assay; the expression of miR-26a-5p, WNT5A, cleavedcaspase3 and Wnt/β-catenin signaling pathway-related proteins in each group was detected using qRT-PCR or Western blot; LDH release, SOD, and GSH-PX activities in each group were detected by kit.

In the H/R group, the expression level of miR-26a-5p was significantly decreased, whereas the expression level of WNT5A was significantly increased. The activity of the Wnt/β-catenin signaling pathway was up-regulated; the level of LDH released was significantly increased; and activities of SOD and GSH-PX were significantly decreased. The aforementioned changes resulted in decreased cell activity and increased apoptosis rate. The overexpression of miR-26a-5p could reduce the expression level of WNT5A, the activity of the Wnt/β-catenin signaling pathway, and the apoptosis rate and restore the cell viability.

These results suggest that miR-26a-5p can target WNT5A and thus, inhibit the Wnt/β-catenin signaling pathway activity, inhibiting H/R-induced cardiomyocyte injury and apoptosis.

本研究旨在探讨miR-26a-5p对缺氧/复氧（H/R）诱导的心肌细胞损伤的作用及其机制。

在大鼠心肌细胞H9c2细胞中构建H/R模型后，细胞中的miR-26a-5p受到干扰（转染miR-26a-5p抑制剂的细胞）或过表达（转染miR-26a-5p模拟物的细胞） . 用CCK-8和流式细胞术检测各组细胞的活力和凋亡率；miR-26a-5p 和 WNT5A 之间的关系通过双荧光素酶报告基因检测得到验证；qRT-PCR或Western blot检测各组miR-26a-5p、WNT5A、cleavedcaspase3和Wnt/β-catenin信号通路相关蛋白的表达；试剂盒检测各组LDH释放、SOD、GSH-PX活性。

在H/R组中，miR-26a-5p的表达水平显着降低，而WNT5A的表达水平显着升高。Wnt/β-catenin信号通路活性上调；释放的LDH水平显着增加；SOD和GSH-PX的活性显着降低。上述变化导致细胞活性降低和细胞凋亡率增加。miR-26a-5p的过表达可降低WNT5A的表达水平、Wnt/β-catenin信号通路的活性和细胞凋亡率，恢复细胞活力。

这些结果表明 miR-26a-5p 可以靶向 WNT5A，从而抑制 Wnt/β-catenin 信号通路活性，抑制 H/R 诱导的心肌细胞损伤和凋亡。