• Qifang Liu, Bo Song, Min Xu, Yaping An, Yidong Zhao, and Feng Yue.
• Department of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China.
• J Chin Med Assoc. 2020 Jan 1; 83 (1): 25-31.

BackgroundWe previously confirmed the targeting of high-mobility group box 1 (HMGB1) by miR-25. This project aims to further investigate whether miR-25 improves myocardial ischemia-reperfusion injury (IRI) in vivo by targeting HMGB1.MethodsA rat model of myocardial IRI was established by the ligation of the left anterior descending coronary artery for 45 minutes followed by 2, 4, or 6 hours reperfusion. The expression of miR-25, HMGB1, and apoptosis-related proteins in the myocardium was determined by quantitative real-time polymerase chain reaction (PCR) and western blotting. The activities of myocardial enzymes and the release of inflammatory cytokines were evaluated by enzyme-linked immunosorbent assay. Evans blue/triphenyltetrazolium chloride double staining was performed to assess infarct size. Myocardial apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling staining.ResultsMiR-25 expression was significantly downregulated, while HMGB1 was highly expressed at the mRNA and protein levels in myocardial tissues after induction of the IRI model. MiR-25 agomir administration suppressed the expression of HMGB1 in myocardial tissues. Furthermore, administration of both miR-25 agomir and lentivirus-mediated short hairpin RNA (shRNA) interference targeting HMGB1 sh-HMGB1 resulted in reduced serum myocardial enzyme activities, cytokine secretion, and myocardial apoptosis during myocardial IRI.ConclusionMiR-25 mitigated myocardial IRI-induced damage by targeting HMGB1.

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