Myocardial ischaemia‐reperfusion (I/R) injury is a serious illness with high morbidity and mortality. Mounting evidence indicates the utility of sevoflurane (SEV) in the treatment of myocardial I/R injury. This study aimed to explore the molecular mechanisms underlying the protective action of SEV against myocardial I/R injury. A rat model of myocardial I/R injury was established, and I/R rats were treated with different concentrations of SEV. MicroRNA‐203 (miR‐203) and doublecortin (DCX) expression levels were determined using reverse transcription‐quantitative polymerase chain reaction. Putative target relationship between miR‐203 and DCX was explored using dual‐luciferase reporter gene assay and RNA‐binding protein immunoprecipitation assay. Ischaemia‐reperfusion rats were treated with SEV, miR‐203 antagomir or sh‐DCX, followed by determination of oxidative stress‐ and inflammation‐related factor levels using nitrite and enzyme‐linked immunosorbent assays, and that of apoptosis‐related factors using Western blot analysis. The apoptotic rate of myocardial tissues was determined using TdT‐mediated dUTP‐biotin nick end labeling (TUNEL) staining, and the infract area was evaluated using triphenyltetrazolium chloride staining. The results showed miR‐203 was poorly expressed and DCX was highly expressed in myocardial tissues of I/R rats. Sevoflurane was found to elevate miR‐203, and miR‐203, in turn, could target and reduce DCX expression. Sevoflurane, miR‐203 overexpression or DCX silencing resulted in declined oxidative stress, inflammation, apoptosis and infarct area, ultimately alleviating myocardial I/R injury. Collectively, these findings showed that SEV‐activated miR‐203 exhibited suppressive effects on myocardial I/R injury in rats and highlighted the SEV/miR‐203/DCX axis as a promising therapeutic target for myocardial I/R injury management.

中文翻译：

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MicroRNA-203 介导的双皮质素抑制支持七氟醚对心肌缺血再灌注损伤后大鼠的心脏保护作用。

心肌缺血再灌注（I/R）损伤是一种严重的疾病，发病率和死亡率都很高。越来越多的证据表明七氟醚 (SEV) 在治疗心肌 I/R 损伤中的效用。本研究旨在探讨 SEV 对心肌 I/R 损伤的保护作用的分子机制。建立大鼠心肌I/R损伤模型，用不同浓度的SEV治疗I/R大鼠。MicroRNA-203 (miR-203) 和双皮质素 (DCX) 的表达水平使用逆转录-定量聚合酶链反应确定。使用双荧光素酶报告基因测定和 RNA 结合蛋白免疫沉淀测定探索 miR-203 和 DCX 之间的假定靶标关系。缺血再灌注大鼠用 SEV、miR-203 antagomir 或 sh-DCX 治疗，然后使用亚硝酸盐和酶联免疫吸附试验确定氧化应激和炎症相关因子水平，并使用蛋白质印迹分析确定细胞凋亡相关因子水平。使用 TdT 介导的 dUTP-生物素缺口末端标记 (TUNEL) 染色测定心肌组织的凋亡率，使用氯化三苯基四唑染色评估梗死面积。结果显示miR-203在I/R大鼠的心肌组织中低表达而DCX高表达。发现七氟烷可以提高 miR-203，而 miR-203 反过来可以靶向并降低 DCX 的表达。七氟烷、miR-203 过表达或 DCX 沉默导致氧化应激、炎症、细胞凋亡和梗死面积下降，最终减轻心肌 I/R 损伤。集体，