Astragaloside IV attenuates apoptosis of hypertrophic cardiomyocyte through inhibiting oxidative stress and calpain-1 activation

被引:62
|
作者
Mei, Meng [1 ]
Tang, Futian [1 ]
Lu, Meili [1 ]
He, Xin [2 ]
Wang, Hongxin [1 ]
Hou, Xuwei [3 ]
Hu, Jin [1 ]
Xu, Chonghua [1 ]
Han, Ronghui [1 ]
机构
[1] Liaoning Med Univ, Inst Drug Res, Key Lab Cardiovasc & Cerebrovasc Drug Res Liaonin, Jinzhou, Liaoning, Peoples R China
[2] Liaoning Med Univ, Affiliated Hosp 1, Internal Med Cardiovasc Dept, Jinzhou, Peoples R China
[3] Liaoning Med Univ, Dept Human Anat, Jinzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
Calpain-1; Oxidation; Apoptosis; Hypertrophy; Astragaloside IV; CARDIAC-HYPERTROPHY; SIGNALING CONTRIBUTES; PATHWAY; ISOPROTERENOL; MITOCHONDRIA; HEART; NOX4; AIF;
D O I
10.1016/j.etap.2015.09.007
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Calpain-1 activation and oxidative stress are two critical factors contributing to apoptosis of hypertrophic cardiomyocyte. Astragaloside IV (ASIV) exhibits protective effect against various heart diseases. The present study was designed to investigate whether the inhibitory effect of ASIV on isoproterenol (ISO)-induced apoptosis of hypertrophic cardiomyocyte was associated with the anti-oxidation and calpain-1 inhibition. Hypertrophy, apoptosis, mitochondrial oxidative stress and calpain-1 expression were measured in the heart tissue of Sprague-Dawley (SD) rats and H9C2 cells treated with ISO alone or combination with ASIV. The results showed that ASIV attenuated apoptotic rate, increased Bcl-2 expression, decreased Bax expression, ameliorated the integrity of mitochondrial structure and improved mitochondrial membrane potential (MMP). Moreover, ASIV combination reduced both calpain-1 protein expression and calpain activity, down-regulated mitochondrial NOX4 (mito-NOX4) expression, increased activity of mitochondrial superoxide dismutase (mito-SOD) and mitochondrial catalase (mito-CAT) compared to ISO treated alone. The results suggested that ASIV exerted anti-apoptosis effect on ISO-induced hypertrophic cardiomyocyte by attenuating oxidative stress and calpain-1 activation. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:764 / 773
页数:10
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