Valsartan improves cardiac function in mice with diabetes mellitus by CaMKII/AngII

To investigate whether valsartan exerts its effect on cardiac function in mice with diabetes mellitus (DM) via Ca2+/calmodulin-dependent protein kinase II (CaMKII).

C57bl6/J mice were used as study subjects and randomly divided into three groups: 1) control group, 2) DM group and 3) valsartan group. After the model was successfully established, the diastolic function in each group of mice was detected via echocardiography, including the ratio of peak velocity blood flow in early diastole to peak velocity blood flow in late diastole (E/A ratio) of mitral valves, isovolumic relaxation time (IVRT) and mitral deceleration time. Ejection fraction (EF), fractional shortening (ES), heart rate (HR) and cardiac output (CO) were determined to evaluate the systolic function of the mouse heart. The frozen heart was stained by dihydroethidium (DHE) and analyzed for the oxidative stress and inflammation levels. The expression levels of phosphorylated calmodulin-dependent protein kinase II (P-CaMKII), oxidized CaMKII (O-CaMKII), ryanodine receptor 2 (RYR2), P-phospholamban (P-PLN) and PLN in tissues were detected via Western blotting.

Valsartan improves myocardial diastolic and systolic function in DM mice by improving phosphorylation and oxidation levels of CaMKII in myocardial cells, and reducing oxidative stress in diabetic cardiomyopathy.

Valsartan could improve CaMKII in myocardial cells to enhance oxidative stress of DM mice, thus improving the cardiac function.