High mobility group?box?1 (HMGB1) protein serves an important role in myocardial ischemia/reperfusion (I/R) injury. MicroRNAs (miRNAs) are a group of small non?coding RNAs that regulate numerous signaling pathways involved in myocardial I/R injury. The present study aimed to investigate whether miR?451 protects against cardiomyocyte anoxia/reoxygenation (A/R) injury by attenuating HMGB1 expression. Neonatal rat ventricular cardiomyocytes were prepared and then subjected to A/R injury. The effect of upregulation or downregulation of miR?451 on cell viability, apoptosis, superoxide dismutase (SOD) activity, and the expression of cleaved?caspase?3 and HMGB1 were measured accordingly. A luciferase assay was performed to further confirm whether miR?451 can directly recognize the 3'?untranslated?region of HMGB1 in HEK293?cells. The expression of miR?451 was significantly decreased in the cardiomyocytes during A/R, and upregulation of miR?451 led to increased miR?451 expression (P<0.05). Upregulation of miR?451 significantly attenuated the loss of cardiomyocyte viability (P<0.05) and increased the intracellular levels of SOD during A/R (P<0.05). Furthermore, upregulation of miR?451 significantly decreased the apoptosis of cardiomyocytes during A/R (P<0.05). The HMGB1 mRNA and protein expression levels were significantly downregulated in the Ad?miR?451 group compared with those in the A/R group (P<0.05). In addition, upregulation of miR?451 reduced its translocation from the nucleus to the cytoplasm. The luciferase assay confirmed that HMGB1 mRNA is a direct target of miR?451 in cardiomyocytes. In conclusion, the present study suggested that upregulation of miR?451 could protect against A/R?induced cardiomyocyte injury by inhibiting HMGB1 expression.

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