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Myocardial diseases usually appear ischemic. Reperfusion therapy is one of the effective methods that can improve clinical therapeutic efficacy. However, reperfusion results in myocardial injury named I/R injury. Rosuvastatin (RS) is HMG-CoA reductase inhibitor. We investigated the role of RS in the myocardial I/R injury in vitro and its active mechanism. Oxygen-glucose deprivation/reoxygenation (OGD/R) model was applied to investigate I/R in vitro . OGD/R decreased cell viability and increased levels of miR-17-3p and lactate dehydrogenase (LDH) leakage. Besides, RS decreased cleaved caspase-3 level and LDH leakage, promoted the levels of miR-17-3p and LC3II/LC3I, and increased cell viability when H9C2 cell was treated by OGD/R. miR-17-3p inhibitor reduced the H9C2 cell viability and LC3II/LC3I level, whereas miR-17-3p mimics increased H9C2 cell viability and LC3II/LC3I level. RS promoted cell viability and increased LC3II/LC3I level while it lowered LDH leakage, apoptosis rate, and the levels of cleaved caspase-3 and Cyto c. Our study suggested that RS reduced I/R injury in cardiocyte via cleaved caspase-3/Cyto c apoptosis signaling pathway and autophagy. Moreover, the autophagy happens to cardiocyte by upregulating the expression of miR-17-3p .

Rosuvastatin Attenuates Myocardial Ischemia-Reperfusion Injury via Upregulating miR-17-3p-Mediated Autophagy