(-)-Epicatechin Inhibits Cardiac Fibrosis via SIRT1/AKT/GSK3β Pathway

Abstract

Background: (-)-Epicatechin (EPI) is an important substance involved in protective effects of flavanol-rich foods. Many studies indicate EPI has cardioprotective effect, but the effect of EPI in inhibition of cardiac fibrosis is unclear. Thus, we aimed to evaluate the effect of EPI in preventing cardiac fibrosis and unveil the molecular mechanisms. Methods: Cardiac fibrosis model was established by transaortic constriction (TAC). The acutely isolated cardiac fibroblasts were induced to myofibroblasts with angiotensin II (AngII). Results: EPI markedly attenuated TAC-induced cardiac dysfunction and fibrosis in mice. In cultured CFs, EPI blocked AngII-induced myofibroblast transformation and collagen production. Furthermore, EPI conducted anti-fibrotic effects by activating the the SIRT1/AKT/GSK3β pathway. Conclusions: These findings will supply new agent and mechanism of action for treating cardiac fibrosis in the future.