(-)-Epicatechin induces physiological cardiac growth by activation of the pi3k/akt pathway in mice

cope : The flavanol (-)-epicatechin has cardioprotective effects and improves physical capacity in normal mice. In addition, (-)-epicatechin increases nitric oxide (NO) production by activation of both PI3K/Akt or Ca2+/CaMI/CaMKII signaling pathways, which have been associated with physiological and pathological cardiac hypertrophy, respectively. Notwithstanding all this information, few studies have been carried out that aimed to determine the potential beneficial effects that (-)-epicatechin may have in normal heart. Methods and results : Mice were treated by oral gavage with the flavanol (-)-epicatechin. The treatment induced a significant increase in heart weight, size of the free walls and size of the cardiac fibers. Also, no evidence of cardiac fibrosis was revealed. Furthermore, the phosphorylation level of PI3K/Akt/mTOR/p70S6K proteins was significantly higher in the heart of (-)-epicatechin-treated animals. In contrast, a significantly decreased level of pathological cardiac hypertrophy markers ANP and BNP was observed along with no modification in the level of β-MHC, CaMI and CaMKII proteins. Hemodynamic parameters indicated an improvement in mechanical heart performance after (-)-epicatechin treatment. Interestingly, morphometric parameters were similar between treated and untreated mice after 4 weeks without treatment. Conclusion : These findings indicate that (-)-epicatechin treatment induced physiological cardiac growth in healthy mice by activation of the PI3K/Akt pathway. This article is protected by copyright. All rights reserved