Fig. 5.
Overexpression of miR-30c attenuated cardiac dysfunction in db/db mice. Db/db mice and C57 control mice were injected with the corresponding rAAVs at 8–10 weeks of age and then sacrificed at 28 weeks of age (n = 8–10). a miR-30c expression was determined by RT-PCR in the heart tissues of mice. b Echocardiographic detection of mice. c Hemodynamic analysis measured by Millar cardiac catheter system of mice. d Representative images and quantitative analysis of oil red O staining of cardiac lipid deposition (bar = 50 μm). e Representative images and quantitative analysis of lipid droplets from cardiac tissues analyzed by transmission electron microscopy (bar = 2 μm). f Representative images and quantification of DHE staining of cardiac ROS production (bar = 50 μm). g Representative images and quantification of TUNEL assay determining cell apoptosis in heart tissues (bar = 100 μm). H. Representative Western blots and quantification of CD36, CPT1B, PDK4, GLUT4 in heart tissues with different treatment. β-actin used as an internal control. Data are expressed as mean ± SEM, *p < 0.05. EF ejection fraction, FS fractional shortening, dP/dtmax peak instantaneous rate of left ventricular pressure increase, dP/dtmin peak instantaneous rate of decline in left ventricular pressure increase, LD lipid droplet