Abstract
AimQi-shen-yi-qi (QSYQ), a formula used for the routine treatment of heart failure (HF) in China, has been demonstrated to improve cardiac function through down-regulating the activation of the Renin-Angiotensin-Aldosterone System (RAAS). However, the mechanisms governing its therapeutic effects are largely unknown. The present study aims to demonstrate that QSYQ treatment can prevent left ventricular remodeling in heart failure by attenuating oxidative stress and inhabiting inflammation.MethodsSprague-Dawley (SD) rats were randomly divided into 6 groups: sham group, model group (LAD coronary artery ligation), QSYQ group with high dosage, middle dosage and low dosage (LAD ligation and treated with QSYQ), and captopril group (LAD ligation and treated with captopril as the positive drug). Indicators of fibrosis (Masson, MMPs, and collagens) and inflammation factors were detected 28 days after surgery.ResultsResults of hemodynamic alterations (dp/dt value) in the model group as well as other ventricular remodeling (VR) markers, such as MMP-2, MMP-9, collagen I and III elevated compared with sham group. VR was accompanied by activation of RAAS (angiotensin II and NADPHoxidase). Levels of pro-inflammatory cytokines (TNF-α, IL-6) in myocardial tissue were also up-regulated. Treatment of QSYQ improved cardiac remodeling through counter-acting the aforementioned events. The improvement of QSYQ was accompanied with a restoration of angiotensin II-NADPHoxidase-ROS-MMPs pathways. In addition, “therapeutic” QSYQ administration can reduce both TNF-α-NF-B and IL-6-STAT3 pathways, respectively, which further proves the beneficial effects of QSYQ.ConclusionsOur study demonstrated that QSYQ protected LAD ligation-induced left VR via attenuating AngII -NADPH oxidase pathway and inhabiting inflammation. These findings provide evidence as to the cardiac protective efficacy of QSYQ to HF and explain the beneficial effects of QSYQ in the clinical application for HF.
Highlights
Heart failure (HF) is the ultimate consequence of a vast number of cardiovascular diseases
HF model group was associated with impaired diastolic and systolic left ventricle (LV) functions, which were largely attenuated by the treatment with QSYQ for 28 d
LV end-diastolic pressure (LVEDP) in model group increased by 81.56%, Min dP/dt was up-regulated by 34.53%, suggesting an injured diastolic function in model rats
Summary
Heart failure (HF) is the ultimate consequence of a vast number of cardiovascular diseases. It is one of the leading causes of morbidity and mortality worldwide [1]. It is considered as an progressive yet irreversible process characterized by damaged pump performance and ventricular remodeling (VR) [2]. Inhabiting VR early is increasingly becoming an effective way to postpone HF induced by myocardial infarction, hypertension and other cardiovascular diseases [4]. Recent clinical studies have indicated that the AngII-induced oxidative stress and inflammation are the critical mechanism of VR.
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