Fig. 5

LCZ696 reduces cardiac remodeling through inhibiting the ERK signaling pathway. PAH mice were treated with sh-ERK with sh-NC as the control, or sh-ERK in the presence of LCZ696 with sh-NC in the presence of LCZ696 or control. a Heart size (scale bar = 100 mm) and ratio of heart weight/body weight in PAH mice. b HE staining of ventricular transection of heart (upper panels: scale bar = 50 mm; lower panels: scale bar = 25 μm). c Cardiomyocyte fibrosis observed by Masson’s trichrome staining (scale bar = 25 μm). d mRNA expression of collagen I, collagen III and TGF-β detected by RT-qPCR. e Isolectin B4 immunofluorescence of the capillary in ventricular tissues (blood vessel: yellow; cell membrane: red; nucleus: blue). f mRNA expression of ANP, βMHC and TIMP2 in cardiomyocytes detected by RT-qPCR. g Apoptosis of cardiomyocytes treated with LCZ696 detected by TUNEL staining (scale bar = 25 μm). h Western blot analysis of ERK protein and extent of ERK phosphorylation. *p < 0.05 vs. PAH mice treated with sh-NC; ^#p < 0.05 vs. PAH mice treated with sh-ERK; ^&p < 0.05 vs. PAH mice treated with sh-NC + LCZ696. N = 7. Measurement data (mean ± S.D.) among multiple groups was analyzed by one-way ANOVA, followed by Tukey post hoc test