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Syringin, extracted from Eleutherococcus senticosus, is a major biologically active component of Chinese herbs. Studies have certified the multiple pharmacological properties of syringin. However, the role of syringin in cardiac hypertrophy and the mechanisms involved remain unclear. In this study, aortic banding was performed on mice in order to induce cardiac hypertrophy, and the animals were then treated with syringin for 7 weeks. Echocardiography and catheter-based measurements of hemodynamic parameters were performed to evaluate cardiac function at 8 weeks following aortic banding. Morphological and pathological changes were also evaluated. Alterations in the expression levels of hypertrophy- and autophagy-related markers [atrial natriuretic peptide (ANP), β-myosin heavy chain MHC), α-MHC, B-type natriuretic peptide (BNP), autophagy-related gene (ATG)5, ATG7, beclin 1, light chain 3 (LC3) A/B] were measured by reverse transcription-quantitative PCR and western blot analysis. The effects of syringin on cardiomyocyte hypertrophy induced by angiotensin II in H9c2 cells were also investigated. The results revealed that syringin attenuated cardiac hypertrophy induced by aortic banding via the activation of AMP-activated protein kinase α (AMPKα) and autophagy-related signaling pathways. Thus, we our data suggest that syringin possesses therapeutic potential to attenuate the progression of cardiac hypertrophy.

Syringin prevents cardiac hypertrophy induced by pressure overload through the attenuation of autophagy