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. 2014 Jun 5;5(6):e1284. doi: 10.1038/cddis.2014.235

Figure 4.

Figure 4

Rho kinase inhibitor fasudil treatment partially improved Rnd3+/− mouse cardiac functions and attenuated apoptotic cardiomyopathy induced by 3-week TAC. (a) Echocardiographic assessment of cardiac functions. (b) A comparison of TUNEL staining in Rnd3 haploinsufficient heart sections among three groups: Sham, TAC only, and TAC plus fasudil treatment. The arrows indicate TUNEL-positive cells (green) overlapped with nucleus counter-staining. Cardiomyocytes were visualized by red fluorescent staining for F-actin. Scale bar represents 10 μm. (c) Quantification of TUNEL staining among the hearts from the three groups. (d) Active and full-length of caspase-3 expression levels among the three groups assessed by immunoblot. (e) Densitometry analysis of active caspase-3 normalized by GAPDH. (f) Phosphorylation levels of Rho kinase substrate MYPT1 among the three groups assessed by immunoblot. (g) Densitometry analysis of MYPT1 phosphorylation. Statistical significance was determined by one-way ANOVA followed by Student–Newman–Keuls method. Data are means±S.D. The number in each column represents the number of mice in the group