Fig. 3: Caspase-1 inhibition attenuates overload-stimulated cardiac hypertrophy.
A1 Representative pictures showing mouse hearts in the indicated groups. A2 Proportion of heart to body weight in the indicated groups. B1 Representative images showing the cross-sectional area of cardiomyocytes of the left ventricle in the indicated groups. Heart tissues were immune-stained with WGA. Green—anti-WGA. One hundred cells were randomly selected from five sections of each heart. Scale bars: 20 μm. B2 Quantification of the cross-sectional area of cardiomyocytes of the left ventricle in the indicated groups. C1 Representative images showing the myocardial fibrosis, assessed using Masson trichrome staining in the indicated groups. Blue areas represent fibrotic staining. Fibrosis was quantified by five whole LV sections for each heart. Scale bars: 50 μm. C2 Quantification of the myocardial fibrosis in the indicated groups. The cardiac structure and function of mice were assessed by echocardiography 4 weeks after TAC. D1 Representative images of M-mode echocardiography for mouse hearts. Quantitative analysis of left ventricular EF (D2), LVEDd (D3), LVEDs (D4), and LVPWd (D5). E Survival curves of mice using Kaplan and Meier. Characteristic images (F1) and measurement (F2) of the cell surface area of cardiomyocytes. Cardiomyocytes were stained with cardiomyocyte marker α-actinin (green fluorescence). Nuclei were marked with DAPI (blue fluorescence), Scale bars: 20 μm. In total, 100 cells were selected on random and assessed for surface area for each cohort from six independent trials. Real-time PCR of mRNA expression of cardiac hypertrophy markers BNP (G) and β-MHC (H). Results are presented as the mean ± SEM, n = 6. ∗P < 0.01 compared to control, #P < 0.01 compared to TAC group, &P < 0.01 compared to Ang-II group.
