Objective: To investigate the effects of rosuvastatin on reactive oxygen species (ROS) production and periostin, cardiotrophin-1 (CT-1) expression, and to explore rosuvastatin on ventricular remodeling in experimental rats after acute myocardial infarction (AMI). Methods: A total of 45 male Wistar rats were randomly divided into 2 group, Sham operation group,n=15 and AMI group,n=30, the AMI model was established by left anterior descending coronary ligation. After 24 hours of AMI, the rats were further divided into 2 groups, AMI + rosuvastatin group, the rats received gastric rosuvastatin 1mg/(kg•d), and AMI group, the rats received gastric normal saline.n=15 in each group and all animals were treated for 6 weeks. The mRNA and protein expressions of CT-1 and periostin were examined by real time RT-PCR and immunohistochemistry, the contents of superoxide anion (O2-·) and hydroxy radical (OH·) were detected by colorimetric method among different groups. Results: Compared with Sham operation group and AMI + suvastatin group, the mRNA and protein expressions of CT-1, periostin, the contents of (O2-·), (OH·) and left heart weight index were increased in AMI group at non-infraction zone,P<005. Compared with Sham operation group, the mRNA and protein expressions of CT-1, periostin, the contents of (O2-·), (OH·) and left heart weight index were increased in AMI + suvastatin group at non-infraction zone,P<005. Compared with AMI group, the mRNA and protein expressions of CT-1 and periostin were decreased in AMI + rosuvastatin group,P<005. Conclusion: Rosuvastatin may improve ventricular remodeling via inhibiting ROS production and CT-1, periostin expression in experimental rats after AMI.%目的：观察大鼠心肌梗死后骨膜蛋白、心肌营养素-1（CT-1）的表达及活性氧物质（ROS）的产生，并用瑞舒伐他汀对其干预，探讨其与心室重塑的关系。方法：45只雄性Wistar大鼠随机分为假手术组（n=15）和心肌梗死组（n=30），通过结扎左冠状动脉前降支（LAD）建立急性心肌梗死模型。模型建立成功24 h后，心肌梗死组再随机分为心肌梗死对照组（n=15）和瑞舒伐他汀干预组（n=15）。瑞舒伐他汀干预组每日给以瑞舒伐他汀1 mg/（kg·d）灌胃，假手术组和心肌梗死对照组每日给予等量生理盐水灌胃，持续6周。利用Real Time 聚合酶链式反应（PCR）法检测非梗死区CT-1、骨膜蛋白 mRNA的表达，免疫组化法测定CT-1、骨膜蛋白的蛋白含量，比色法分别测定标本中超氧阴离子（O2-·）及羟自由基（OH·）的含量。结果：给药6周后，心肌梗死对照组相比假手术组、瑞舒伐他汀干预组非梗死区心肌中CT-1 mRNA、骨膜蛋白 mRNA的表达、CT-1及骨膜的蛋白含量、超氧阴离子（O2-·）及羟自由基（OH·）含量、左心室重量指数显著升高（P<0.05），差异有统计学意义；瑞舒伐他汀干预组与假手术组相比，非梗死区心肌中CT-1 mRNA、骨膜蛋白 mRNA的表达、CT-1及骨膜蛋白的蛋白含量、超氧阴离子（O2-·）及羟自由基（OH·）含量、左心室重量指数显著升高（P<0.05），差异有统计学意义。瑞舒伐他汀干预组与心肌梗死对照组相比，CT-1及骨膜蛋白 mRNA表达和蛋白含量明显下降（P<0.05），差异有统计学意义。结论：瑞舒伐他汀可能通过抑制ROS产生、CT-1及骨膜蛋白在mRNA和蛋白水平的表达来改善大鼠心肌梗死后心室重塑。
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