Objective The inhaled sevoflurane has been demonstrated to protect against myocardial ischemia/reperfusion (I/R) injury. However, the relative mechanisms of sevoflurane‐mediated cardioprotection remain largely unknown. This study intends to explore the effect of miR‐155 on the sevoflurane‐mediated cardioprotection by regulating Sirtuin 1 (SIRT1) in mouse models of myocardial I/R. Methods Left anterior descending coronary artery ligation was used to induce models of myocardial I/R in mice. The I/R mice were treated with sevoflurane, sevoflurane + mimics negative control (NC) or sevoflurane + miR‐155 mimics. The expression of microRNA‐155 (miR‐155) and SIRT1 was examined by quantitative real‐time polymerase chain reaction and Western blot assay. Then cardiac functions and hemodynamic alterations were evaluated. Evans blue‐2,3,5‐triphenyltetrazolium chloride and terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling assay staining methods were adopted to evaluate infarct size and cardiomyocyte apoptosis, respectively. Results In the I/R mice, miR‐155 was expressed at a high level and SIRT1 at a low level. SIRT1 was confirmed to be a target gene of miR‐155. The treatment of sevoflurane could reduce miR‐155 expression and increased SIRT1 expression in the myocardial tissues, under which conditions, cardiac functions were promoted, accompanied by reduced infarct size and inhibited cardiomyocyte apoptosis. In response to miR‐155 upregulation, the sevoflurane‐treated I/R mice showed reduced cardiac functions, and increased infarct size and cardiomyocyte apoptosis. Conclusion The findings obtained in this study provide evidence suggesting that miR‐155 targets and negatively regulates SIRT1 expression, a mechanism by which the protection of sevoflurane is inhibited against myocardial I/R in mice.

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