title: Syringin prevents cardiac hypertrophy induced by pressure overload through the attenuation of autophagy.
abstract: 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.
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Fangfang
authors.initials: F
authors.lastname: Li
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Ning
authors.initials: N
authors.lastname: Zhang
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Qingqing
authors.initials: Q
authors.lastname: Wu
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Yuan
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Zheng
authors.initials: Z
authors.lastname: Yang
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Mengqiao
authors.initials: M
authors.lastname: Zhou
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Jinxiu
authors.initials: J
authors.lastname: Zhu
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
authors.forename: Qizhu
authors.initials: Q
authors.lastname: Tang
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D000804:Angiotensin II; D000818:Animals; D001343:Autophagy / Q000187:drug effects*; D006332:Cardiomegaly / Q000188:drug therapy* / Q000473:pathology / Q000517:prevention & control*; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002460:Cell Line; D005960:Glucosides / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D008810:Mice, Inbred C57BL; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D010666:Phenylpropionates / Q000494:pharmacology / Q000627:therapeutic use*; D011312:Pressure; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D002316:Cardiotonic Agents; D005960:Glucosides; D010666:Phenylpropionates; D000804:Angiotensin II; D055372:AMP-Activated Protein Kinases; C028305:syringin