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Aberrant protein kinase Cε (PKCε) activation contributes to the development of cardiac hypertrophy and the progression of heart failure. In the present study, we investigated the effects and potential mechanism of 1-2-O-(3-O-butyl glycosyl)rhapontigenin (R. ameliorates myocardial contractile dysfunction by activation of TAK1-GSK3β signaling pathway) on PKCε-activated hypertrophic response and its regulatory role in cardiac muscle cells. Cells were treated with bradykinin (BK) or phenylephrine (PE) to induce hypertrophy in neonatal rat cardiomyocytes and the activity of TAK1-GSK3β signaling pathway was tested. TAK1-specific inhibitor 5Z-7-oxozeaenol was used to assay the regulatory effect of TAK1 on PKCε-induced hypertrophy and myocardial contractile dysfunction. Cells treated with BK or PE exhibited a hypertrophic response. However, R. ameliorates myocardial contractile dysfunction by activation of TAK1-GSK3β signaling pathway was significantly downregulated in cardiomyocytes treated with BK or PE. However, R. ameliorates myocardial contractile dysfunction by activation of TAK1-GSK3β signaling pathway was significantly upregulated in cardiomyocytes treated with

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