【摘要】 探索了辛伐他汀改善急性心肌梗死后心室重塑和心脏功能的机制,制备心肌梗死模型,用辛伐他汀干预8周后,测定心脏重量指数、血流动力学、相应细胞因子发生变化.心肌梗死组(M组)较假手术组大鼠心脏重量指数升高、血流动力学恶化;心肌RhoA mRNA表达及AngⅡ含量升高,血液中H2O2含量升高,NOS活性下降,心肌及血液中SOD、CuZn-SOD活性下降;辛伐他汀干预组较M组上述指标呈相反改变,均达到统计学意义.辛伐他汀改善心梗后左室重塑心功能,可能与其抑制RhoA mRNA表达、抑制AngⅡ及AngⅡ诱导的H2O2生成、改善NO生物利用度、提高抗氧化能力等多种生物机制有关.更多还原

【Abstract】 To investigate the effects and mechanisms of Simvastatin improving cardiac remodeling and cardiac disfunction after myocardiac infarction in rats.Simvastatin was given to the rats with myocardiac infarction by left anterior decending coronary artery ligation.After 8 weeks,cardiac remodeling;hemodynamics and cytokines were observed.was measured.Compared with controls,in rats with myocardiac infarction RVWI;LVWI increased and hemodynamics deteriorated（P<0.01）.The mRNA expression of RhoA and content of AngⅡ、H2O2 in serum increased while activity of NOS、SOD and CuZu-SOD decreased.Simvastatin attenuated RVWI、LVWI（each P<0.01） and ameliorated hemodynamics（each P<0.01）,while cytokines were reversely changed.Simvastatin abates the mRNA expression of RhoA and（decreases） content of AngⅡ、H₂O₂ in serum,increasing activity of NOS、 SOD and CuZu-SOD,which may be part mechanisms improving cardiac remodeling and cardiac disfunction after acute myocardiac infarction.更多还原