Abstract
The aim was to examine the role of exogenous hydrogen sulfide (H2S) on cardiac remodeling in post-myocardial infarction (MI) rats. MI was induced in rats by ligation of coronary artery. After treatment with sodium hydrosulfide (NaHS, an exogenous H2S donor, 56 μM/kg·day) for 42 days, the effects of NaHS on left ventricular morphometric features, echocardiographic parameters, heme oxygenase-1 (HO-1), matrix metalloproteinases-9 (MMP-9), type I and type III collagen, vascular endothelial growth factor (VEGF), CD34, and α-smooth muscle actin (α-SMA) in the border zone of infarct area were analyzed to elucidate the protective mechanisms of exogenous H2S on cardiac function and fibrosis. Forty-two days post MI, NaHS-treatment resulted in a decrease in myocardial fibrotic area in association with decreased levels of type I, type III collagen and MMP-9 and improved cardiac function. Meanwhile, NaHS administration significantly increased cystathionine γ-lyase (CSE), HO-1, α-SMA, and VEGF expression. This effect was accompanied by an increase in vascular density in the border zone of infarcted myocardium. Our results provided the strong evidences that exogenous H2S prevented cardiac remodeling, at least in part, through inhibition of extracellular matrix accumulation and increase in vascular density.
Highlights
Peripheral artery disease is an important healthcare problem in the world and is associated with increased risk for coronary artery events, such as myocardial infarction (MI) [1,2]
In agreement with our previous study showing that NaHS administration could reduce the fibrosis size in heart failure rats [21], the extent of fibrosis significantly reduced in the NaHS treatment group
(15.0% ± 3.2%) compared with vehicle group (32.8% ± 1.4%) (Figure 1C, p < 0.05). These findings suggested that NaHS might attenuate extracellular matrix accumulation in the border zone of infarcted myocardium
Summary
Peripheral artery disease is an important healthcare problem in the world and is associated with increased risk for coronary artery events, such as myocardial infarction (MI) [1,2]. Adverse cardiac remodeling following MI remains a significant cause of congestive heart failure [3]. Cardiac remodeling is characterized by significant changes in left ventricle size, shape, and function [4]. This myocardial remodeling sets in motion a number of cellular and extracellular matrix events. The extracellular matrix turnover in the non-ischemic myocardium is considered to be maladaptive and contributes to the pathophysiology of myocardial remodeling and progression to heart failure [5,6]. Induction and/or activation of matrix metalloproteinases (MMPs) in the surrounding viable myocardium accelerate extracellular matrix turnover and a failure of mature scar formation [7]
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