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

INTRODUCTION
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
Ten μM aspirin significantly inhibited Ang II-induced increase in cardiomyocyte size, the mRNA, and protein levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and β-myosin heavy chain (β-MHC) (P < 0.05). Meantime, consistent with the result in vitro, the increase in 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, left ventricular end-diastolic dimensions, and left ventricular end-systolic dimensions were significantly decreased (P < 0.05), whereas interventricular septal thickness at end-diastole, interventricular septal thickness at end-systole, posterior wall thickness in diastole, and posterior wall thickness in systole were markedly increased (P < 0.05), which could be reversed by aspirin (P < 0.05). Moreover, aspirin blunted the increase inCa(2+) 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 Ca(2+)/calcineurin-NFAT signaling pathway. Therefore, these findings suggested that aspirin might become a therapeutic option to reduce cardiac hypertrophy.