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Fig. 4 | Cell & Bioscience

Fig. 4

From: Angiotensin II receptor blocker LCZ696 attenuates cardiac remodeling through the inhibition of the ERK signaling pathway in mice with pregnancy-associated cardiomyopathy

Fig. 4

LCZ696 diminishes cardiac hypertrophy and fibrosis induced by Ang II via suppression of the ERK phosphorylation. Cardiomyocytes were initially treated with either sh-NC or sh-ERK, or without any treatment. a mRNA and protein expression of ERK detected by RT-qPCR and western blot analysis. b Western blot analysis of the extent of ERK phosphorylation in cardiomyocytes upon different treatment. c Cardiac hypertrophy condition assessed by 3[H]-leucine incorporation methodology. d mRNA expression of ANP, βMHC and TIMP2 in cardiomyocytes detected by RT-qPCR. E, Cardiomyocyte fibrosis assessed by 3[H]-proline incorporation methodology. F, mRNA expression of collagen I, collagen III and TGF-β probed by RT-qPCR. G, Apoptosis of cardiomyocytes treated with LCZ696 as probed by TUNEL staining (scale bar = 25 μm). *p < 0.05 vs. cardiomyocytes without treatment; #p < 0.05 vs. cardiomyocytes treated with control + Ang II; &p < 0.05 vs. cardiomyocytes treated with Ang II + sh-NC; @p < 0.05 vs. cardiomyocytes treated with Ang II + sh-ERK; $p < 0.05 vs. cardiomyocytes treated with Ang II + sh-NC + LCZ696. Measurement data (mean ± S.D.) among multiple groups was analyzed by one-way ANOVA, followed by Tukey post hoc test. The experiment was conducted 3 times independently

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