LCZ696 Ameliorates Oxidative Stress and Pressure Overload-Induced Pathological Cardiac Remodeling by Regulating the Sirt3/MnSOD Pathway

Figure 6

LCZ696 blocked the hypertrophic response in NRCMs. (a) Immunofluorescence staining of sarcomeric alpha-actinin (α-actinin) in primary neonatal rat cardiomyocytes (NRCMs) in the indicated treatment groups. (b) The cell surface area of the indicated groups ( cells per experimental group). (c) mRNA levels of ANP, BNP, and β-MHC in different treatment groups. The results were normalized against GAPDH and converted to fold change relative to the ctrl group. (d) Intracellular ROS levels in primary cardiomyocytes were quantified with DCFH-DA staining. (e) Mitochondrial ROS levels in primary cardiomyocytes were measured by MitoSOX staining. (f) Representative TUNEL staining of primary cardiomyocytes in different treatment groups. Data are presented as . vs. the control group, ^# vs. the PE treatment group.

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