MicroRNAs have been reported to be implicated in myocardial ischemia/reperfusion (I/R) injury. The purpose of this study was to investigate the effect of miR‐183‐5p on I/R injury. Overexpression of miR‐183‐5p by agomiR transfection alleviated cardiac dysfunction and significantly reduced the infarct size in rats with myocardial I/R. MiR‐183‐5p also alleviated myocardial apoptosis with reduced apoptotic cells and lower levels of apoptosis associated proteins. in vitro experiments were conducted on rat H9c2 cells treated with anoxia/reoxygenation (A/R). Annexin V/propidium iodide (PI) staining and flow cytometry reported that the ratio of apoptotic cells decreased by miR‐183‐5p transfection before A/R treatment. Moreover, according to binding sequence prediction and Dual luciferase reporter assay, we explored that voltage‐dependent anion channel 1 (VDAC1), which aggravates myocardial injury and apoptosis reported in our former research, was a target of miR‐183‐5p. In conclusion, miR‐183‐5p can efficiently attenuate I/R injury and miR‐183‐5p may exert its effect through repressing VDAC1 expression.

中文翻译：

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MiR-183-5p通过靶向VDAC1保护大鼠心脏免遭心肌缺血/再灌注损伤。

据报道，MicroRNA与心肌缺血/再灌注（I / R）损伤有关。这项研究的目的是研究miR‐183‐5p对I / R损伤的影响。agomiR转染使miR‐183-5p过度表达可减轻心脏功能障碍，并显着减少患有心肌I / R的大鼠的梗塞面积。MiR-183-5p还通过减少凋亡细胞和降低凋亡相关蛋白的水平来减轻心肌凋亡。在用缺氧/复氧（A / R）处理的大鼠H9c2细胞上进行了体外实验。Annexin V /碘化丙啶（PI）染色和流式细胞术报告说，在进行A / R治疗之前，miR‐183-5p转染可导致凋亡细胞比例降低。此外，根据结合序列预测和双重荧光素酶报告基因分析，我们探讨了电压依赖性阴离子通道1（VDAC1）是miR-183-5p的靶点，该通道加剧了我们先前研究中报道的心肌损伤和细胞凋亡。总之，miR‐183‐5p可以有效减轻I / R损伤，miR‐183‐5p可能通过抑制VDAC1表达发挥作用。