QSYQ Attenuates Oxidative Stress and Apoptosis Induced Heart Remodeling Rats through Different Subtypes of NADPH-Oxidase

We aim to investigate the therapeutic effects of QSYQ, a drug of heart failure (HF) in clinical practice in China, on a rat heart failure (HF) model. 3 groups were divided: HF model group (LAD ligation), QSYQ group (LAD ligation and treated with QSYQ), and sham-operated group. After 4 weeks, rats we...

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Published in:Evidence-based complementary and alternative medicine 2013-01, Vol.2013 (2013), p.1-8
Main Authors: Wang, Yong, Li, Chun, Ouyang, Yuli, Shi, Tianjiao, Yang, Xiaomin, Yu, Junda, Qiu, Qi, Han, Jing, Wu, Yan, Tang, Binghua, Wang, Wei
Format: Article
Language:English
Subjects:
Angiotensin II
Apoptosis
Biology
Cardiology
Cardiovascular disease
Caspase
Caspase-3
CYBB protein
Free radicals
Gelatinase A
Hafnium
Heart diseases
Heart failure
Hypertrophy
Integrative medicine
Laboratory animals
Malondialdehyde
Medicine
NAD(P)H oxidase
NOX4 protein
Oxidative stress
p53 Protein
Pathology
Physiology
Rats
Reactive oxygen species
Tumor necrosis factor-TNF
Ventricle
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Summary:We aim to investigate the therapeutic effects of QSYQ, a drug of heart failure (HF) in clinical practice in China, on a rat heart failure (HF) model. 3 groups were divided: HF model group (LAD ligation), QSYQ group (LAD ligation and treated with QSYQ), and sham-operated group. After 4 weeks, rats were sacrificed for cardiac injury measurements. Rats with HF showed obvious histological changes including necrosis and inflammation foci, elevated ventricular remodeling markers levels(matrix metalloproteinases-2, MMP-2), deregulated ejection fraction (EF) value, increased formation of oxidative stress (Malondialdehyde, MDA), and up-regulated levels of apoptotic cells (caspase-3, p53 and tunnel) in myocardial tissue. Treatment of QSYQ improved cardiac remodeling through counter-acting those events. The improvement of QSYQ was accompanied with a restoration of NADPH oxidase 4 (NOX4) and NADPH oxidase 2 (NOX2) pathways in different patterns. Administration of QSYQ could attenuate LAD-induced HF, and AngII-NOX2-ROS-MMPs pathway seemed to be the critical potential targets for QSYQ to reduce the remodeling. Moreover, NOX4 was another key targets to inhibit the p53 and Caspase3, thus to reduce the hypertrophy and apoptosis, and eventually provide a synergetic cardiac protective effect.
ISSN:1741-427X
1741-4288
DOI:10.1155/2013/824960