Effects of stachydrine on norepinephrine-induced neonatal rat cardiac myocytes hypertrophy and intracellular calcium transients

BMC Complementary and Alternative Medicine

Research Article

Xiao-Li Shan¹  Pei Zhao¹  Hong-Chang Wei¹  Wei Guo¹  Chen Zhang¹  Rong Lu¹  Yue-Ling Liao¹ 

[1] Department of Pathology, Shanghai University of Traditional Chinese Medicine, 201203, Shanghai, China;

关键词: Ca transients;    Cardiac hypertrophy;    Phospholamban;    SERCA2a;    Stachydrine;   

DOI  :  10.1186/1472-6882-14-474

 received in 2014-08-04, accepted in 2014-11-27,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundLeonurus heterophyllus sweet has been suggested to have cardioprotective effects against heart diseases, including ischemic diseases and ventricular remodeling. However, the active ingredients of the herb and the underlying mechanisms are poorly understood. The aim of the present study was to investigate the effects of stachydrine (STA), a major constituent of Leonurus heterophyllus sweet, on norepinephrine (NE) induced hypertrophy and the changes of calcium transients in neonatal rat cardiomyocytes.MethodsVentricular myocytes from 1-day-old Wistar rats were isolated and cultured in DMEM/F12 with 1 μmol/L norepinephrine in the presence or absence of 10 μmol/L STA for 72 h. Cardiomyocytes hypertrophy was evaluated by cell surface area, total protein/DNA content, β/α-MHC mRNA ratio. While calcium handling function was evaluated by Ca2+-transient amplitude and decay, SERCA2a activity and expression, PLN expression and phosphorylation. β1-adrenergic receptor system activation was evaluated by the content of cAMP and the activation of PKA.ResultsNE treatment increases the cell surface area, protein synthesis, the expression level of β-MHC and β/α-MHC ratio. These effects were attenuated by STA. NE-induced hypertrophy was associated with increased Ca2+-transient amplitude, accelerated decay of the Ca2+-transient, increased phospholamban expression, hyper-phosphorylation at both the serine-16 and threonine-17 residues, increased intracellular cAMP level, and PKA overactivation. All of which were significantly inhibited by STA.ConclusionThese data suggest that STA attenuates norepinephrine-induced cardiomyocyte hypertrophy and has potential protective effects against β-adrenergic receptor induced Ca2+ mishandling.

【 授权许可】

Unknown   
© Zhang et al.; licensee BioMed Central. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.