Research Article QSYQ Attenuates Oxidative Stress and Apoptosis Induced Heart Remodeling Rats through Different

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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 4weeks, ratswere sacrificed for cardiac injurymeasurements. RatswithHF showedobvious 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) inmyocardial tissue. Treatment ofQSYQ improved cardiac remodeling through counter-acting those events.The improvement of QSYQwas accompanied with a restoration of NADPHoxidase 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 forQSYQ 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. 1