Hydrogen Sulfide Endothelin-Induced Myocardial Hypertrophy in Rats and the Mechanism Involved

Abstract

The aim of the study was to evaluate the clinical efficacy of hydrogen sulfide (H2S) treatment on the endothelin-induced cardiac hypertrophy. Sixty-four adult male rats, weighing from 180 to 200 g, were randomly divided into four groups: ten in normal group, ten in sham group, 44 in model group established by inducing the myocardial hypertrophy with endothelin. The myocardial hypertrophy model rats were randomly divided into two groups: 22 in the simple myocardial hypertrophy model group and 22 in the H2S treatment group. Rats in normal group were given 2 ml pure water by gavage per day, those in the sham group and simple cardiac hypertrophy model group were given 2 ml of saline by gavage per day, and rats in the pure cardiac hypertrophy with H2S treatment were given intraperitoneal injections of 2 ml NaHS saline per day for a period of 4 weeks. Left ventricular mass index, myocyte hypertrophy, volume fraction of myocardial interstitial collagen, myocardial hydroxyproline content and other indicators of cardiac hypertrophy were observed after 4 weeks. (1) There were significant differences on the ventricular mass between the treatment group and the cardiac hypertrophy group: The left ventricular mass decreased 21.4 % and the left ventricular mass index decreased 5.97 % (P < 0.05; (2) the smallest cardiomyocytes diameter and cardiomyocytes cross-sectional area decreased 12.5 and 10.8 %, respectively (P < 0.05) in the treatment group compared to the cardiac hypertrophy group; (3) the volume fraction of myocardial interstitial collagen and the myocardial hydroxyproline content decreased 22.3 and 31.3 % in treatment group compared with the cardiac hypertrophy group, respectively (P < 0.05). H2S had a good clinical efficacy in reducing left ventricular mass fraction and myocardial collagen levels, improving myocardial hypertrophy and decrease myocardial fibrosis. It is worthy for further clinical studies.

The Cardioprotective Effects of Hydrogen Sulfide in Heart Diseases: From Molecular Mechanisms to Therapeutic Potential

“…In addition, pharmacologic H 2 S therapy during heart failure serves to mitigate pathological left ventricular remodeling and reduce myocardial hypertrophy, oxidative stress, and apoptosis [ 49 ]. In an endothelin-induced cardiac hypertrophy rat model, Yang et al [ 57 ] found that H 2 S treatment could decrease left ventricular mass index, volume fraction of myocardial interstitial collagen, and myocardial collagen content and improve cardiac hypertrophy. In another hypertrophy model induced by abdominal aorta coarctation, Huang et al [ 58 ] revealed that exogenous administration of H 2 S significantly suppressed the development of cardiac hypertrophy and also greatly downregulated the Ang-II levels in cardiac tissue, suggesting that H 2 S plays a pivotal role in the development of pressure overload-induced cardiac hypertrophy.…”

Hydrogen sulfide pretreatment improves mitochondrial function in myocardial hypertrophy via a SIRT3‐dependent manner

“…H 2 S attenuated phenylephrine‐induced cardiomyocyte hypertrophy via improved glucose metabolism or up‐regulation of mir‐133 (Liu et al , ; Liang et al , ). H 2 S also prevented endothelin‐ or smoking‐induced enhancement of left ventricular mass (Yang et al , ; Zhou et al , ). H 2 S attenuated myocardial hypertrophy induced by abdominal aortic constriction in rats, through connexin 43 up‐regulation (Huang et al , ).…”

Hydrogen Sulfide Inhibits High-Salt Diet-Induced Myocardial Oxidative Stress and Myocardial Hypertrophy in Dahl Rats

“…Studies showed that H 2 S had a protective effect on myocardial injury in different diseases (Liu et al, 2014; Shen et al, 2015). H 2 S protected the myocardium and cardiac function by inhibiting inflammatory reaction and apoptosis, etc (Sodha et al, 2009; Su et al, 2009; Wei et al, 2010; Lu et al, 2013; Yang et al, 2014). Furthermore, our previous studies demonstrated that down-regulation of renal H 2 S/CBS pathway induced by high salt led to the development of hypertension, and H 2 S could improve aortic structural remodeling and reduce the high salt-induced renal injury in Dahl rats (Huang et al, 2015, 2016), suggesting that the effect of H 2 S on the function and structure of aorta and kidney participated in the protective regulation of H 2 S on the myocardial hypertrophy.…”