Aspirin Attenuates Angiotensin II-induced Cardiomyocyte Hypertrophy by Inhibiting the Ca 2+ /Calcineurin-NFAT Signaling Pathway

In this study, we examined whether aspirin could inhibit cardiac hypertrophy. Methods：We utilized cultured neonatal mouse cardiomyocytes and mice for the study and subjected to cardiomyocyte immunochemistry, qRT-PCR and immunoblotting analysis. The cardiac function was measured using M-mode echocardiography. Results: 10 µM aspirin significantly inhibited Ang II-induced increase of cardiomyocyte size, the mRNA and protein levels of ANP, BNP and β-MHC (P<0.05). Meantime, consistent with the result in vitro, the increase of HW/BW ratio, the mRNA and protein levels of ANP, BNP and β-MHC could be reduced by aspirin in vivo (P<0.05). Analysis of cardiac function revealed that mouse hearts treated with Ang II displayed thickening of the ventricular walls, LVEDD and LVESD were significantly decreased (P<0.05), while IVSTD, IVSTS, PWTD and PWTS were markedly increased (P<0.05), which could be reversed by aspirin (P<0.05). Moreover, aspirin blunted the increase of Ca2+ and inhibited the calcineurin activity and NFAT dephosphorylation caused by Ang II (P<0.05). Conclusions: Aspirin inhibited cardiac hypertrophy in vitro and in vivo through inhibition of the Ca2+/calcineurin–NFAT signaling pathway. Therefore, these findings suggested that aspirin might become a therapeutic option to reduce cardiac hypertrophy.