摘要：C57BL/6 mice with dilated cardiomyopathy (DCM) were randomly divided to receive placebo or pitavastatin at a dose of 1 or 3 mg kg–1d–1.After 8 weeks treatment,mice with dilated cardiomyopathy developed serious cardiac dysfunction characterized by significantly enhanced left ventricular end-diastolic diameter (LVIDd),decreased left ventricular ejection fraction (LVEF) as well as left ventricular short axis fractional shortening (LVFS),accompanied with enlarged cardiomyocytes,and increased plasma levels of N-terminal pro-B type natriuretic peptide (NT-proBNP) and plasma angiotensin II (AngII) concentration.Moreover,myocardium sarcoplasmic reticulum Ca2+ pump (SERCA-2) activity was decreased.The ratio of phosphorylated phospholamban (PLB) to total PLB decreased significantly with the down-regulation of SERCA- -2a and ryanodine receptor (RyR2) expression.Pitavastatin was found to ameliorate the cardiac dysfunction in mice with dilated cardiomyopathy by reversing the changes in the ratios of phosphorylated PLB to total PLB,SERCA-2a and RyR2 via reducing the plasma AngII concentration and the expressions of myocardium angiotensin II type 1 receptor (AT1R) and protein kinase C (PKC)b2.The possible underlying mechanism might be the regulation of myocardial AT1R-PKCb2-Ca2+ handling proteins.
