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.