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.

中文翻译：

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罗苏伐他汀通过上调miR-17-3p介导的自噬来减轻心肌缺血-再灌注损伤。

心肌疾病通常表现为缺血性。再灌注疗法是可以提高临床疗效的有效方法之一。但是，再灌注会导致心肌损伤，称为I / R损伤。罗苏伐他汀（RS）是HMG-CoA还原酶抑制剂。我们调查了RS在体外心肌I / R损伤中的作用及其活性机制。氧-葡萄糖剥夺/复氧（OGD / R）模型用于体外研究I / R。OGD / R降低细胞活力，并增加miR-17-3p和乳酸脱氢酶（LDH）泄漏的水平。此外，当用OGD / R处理H9C2细胞时，RS降低了裂解的caspase-3水平和LDH泄漏，提高了miR-17-3p和LC3II / LC3I的水平，并提高了细胞活力。miR-17-3p抑制剂降低了H9C2细胞的活力和LC3II / LC3I水平，而miR-17-3p模拟物可提高H9C2细胞的活力和LC3II / LC3I水平。RS促进细胞活力并增加LC3II / LC3I水平，同时降低LDH渗漏，凋亡率以及裂解的caspase-3和Cyto c的水平。我们的研究表明，RS通过裂解caspase-3 / Cyto c凋亡信号通路和自噬减少了心肌的I / R损伤。此外，通过上调miR-17-3p的表达，自噬发生在心肌细胞上。