Puerarin prevents cardiac hypertrophy induced by pressure overload through activation of autophagy

被引:75
作者
Liu, Bei [1 ]
Wu, Zhiye [1 ]
Li, Yunpeng [1 ]
Ou, Caiwen [1 ]
Huang, Zhenjun [2 ]
Zhang, Jianwu [1 ]
Liu, Peng [1 ]
Luo, Chengfeng [2 ]
Chen, Minsheng [1 ]
机构
[1] Southern Med Univ, Zhujiang Hosp, Dept Cardiol, Guangzhou 510280, Guangdong, Peoples R China
[2] Guangzhou Med Univ, Affiliated Hosp 2, Dept Cardiol, Guangzhou 510260, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Puerarin; Cardiac hypertrophy; Autophagy; AMPK; HEMODYNAMIC STRESS; EXPRESSION; DISEASE; CELLS; MICE;
D O I
10.1016/j.bbrc.2015.07.065
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This study aimed to explore the effects of puerarin on autophagy in cardiac hypertrophy. Decreased 5'-adenosine monophosphate kinase (AMPK) activity alone with inhibited autophagy could be detected in rats within 3 weeks after aortic banding (AB). Puerarin treatment for 3 weeks in AB rats significantly restored autophagy. Administration of puerarin for 6 weeks effectively restricted cardiomyocyte hypertrophy and apoptosis. In an in vitro study, similar anti-hypertrophy and anti-apoptosis effects of puerarin on isoprenaline-induced H9c2 cells were also observed. After inhibition of autophagy by pretreatment with 3-methyladenine, the protective effects of puerarin were blocked. Further in vivo study demonstrated that puerarin significantly enabled phosphorylation of 5'-AMPK to be activated, subsequently inhibiting expression of the mammalian target of rapamycin (mTOR) target proteins S6 ribosomal protein and 4E-binding protein 1. All these data indicate that puerarin exerts protective effects against cardiomyocyte hypertrophy and apoptosis, partly by restoration of autophagy through AMPK/mTOR-mediated signaling. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:908 / 915
页数:8
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