Fig. 5: SIRT1 knockout blocked the cardioprotective effect of CTRP3 in TAC mice.

A Representative western blotting of SIRT1 protein level in the heart tissues of SIRT1-KO mice. GAPDH serves as a loading control. B Top panel, representative echocardiographic images 4 weeks after TAC surgery. Bottom two panels, LVEF and LVFS determined by analyzing echocardiographic images (n = 10). C Left panel, representative images of heart sections stained with HE and Masson’s trichrome. Right panel, quantification of left ventricular cross-sectional area and collagen volume (n = 5, 10–15 random fields were analyzed per sample). D Representative western blotting and quantification of β-MHC, ANP, collagen-1, and α-SAM protein levels in heart tissues. GAPDH served as a loading control (n = 4). E Representative western blotting and quantification of ATF5, ClpP, Lonp1, HSP10, and HSP60 protein levels in heart tissues. GAPDH served as a loading control (n = 4). F Top panel, representative electron microscope images of a cardiomyocyte mitochondrion of the heart. Bottom two panels, quantification of mitochondria density, cristae/mitochondrial area in heart tissues (n = 5, 10–15 random fields were analyzed per sample). G Quantification of ATP levels in heart tissues (n = 5). H Left panel, representative fluorescence images of cardiac sections stained with DHE (red) to indicate ROS levels; nuclei were stained with DAPI (blue). Right panel, relative quantification of ROS fluorescence intensity in heart tissues (n = 6, 10–15 random fields were analyzed per sample). I Quantification of MDA levels in heart tissues (n = 10). J Quantification of SOD activities in heart tissues (n = 10). Data were analyzed by one-way ANOVA and presented as mean ± SEM. ^*P < 0.05; ^**P < 0.01; ^***P < 0.001; ns not significant, LVEF left ventricular ejection fraction, LVFS left ventricular fraction shortening, MDA malondialdehyde, TAC transverse aortic constriction.