Abstract
The study aimed to examine the protective effect of hydrogen sulfide (H2S) on high-salt-induced oxidative stress and myocardial hypertrophy in salt-sensitive (Dahl) rats. Thirty male Dahl rats and 40 SD rats were included in the study. They were randomly divided into Dahl control (Dahl + NS), Dahl high salt (Dahl + HS), Dahl + HS + NaHS, SD + NS, SD + HS, SD + HS + NaHS, and SD + HS + hydroxylamine (HA). Rats in Dahl + NS and SD + NS groups were given chow with 0.5% NaCl and 0.9% normal saline intraperitoneally daily. Myocardial structure, α-myosin heavy chain (α-MHC) and β-myosin heavy chain (β-MHC) expressions were determined. Endogenous myocardial H2S pathway and oxidative stress in myocardial tissues were tested. Myocardial H2S pathway was downregulated with myocardial hypertrophy featured by increased heart weight/body weight and cardiomyocytes cross-sectional area, decreased α-MHC and increased β-MHC expressions in Dahl rats with high-salt diet (all P < 0.01), and oxidative stress in myocardial tissues was significantly activated, demonstrated by the increased contents of hydroxyl radical, malondialdehyde and oxidized glutathione and decreased total antioxidant capacity, carbon monoxide, catalase, glutathione, glutathione peroxidase, superoxide dismutase (SOD) activities and decreased SOD1 and SOD2 protein expressions (P < 0.05, P < 0.01). However, H2S reduced myocardial hypertrophy with decreased heart weight/body weight and cardiomyocytes cross-sectional area, increased α-MHC, decreased β-MHC expressions and inhibited oxidative stress in myocardial tissues of Dahl rats with high-salt diet. However, no significant difference was found in H2S pathway, myocardial structure, α-MHC and β-MHC protein and oxidative status in myocardial tissues among SD + NS, SD + HS, and SD + HS + NaHS groups. HA, an inhibitor of cystathionine β-synthase, inhibited myocardial H2S pathway (P < 0.01), and stimulated myocardial hypertrophy and oxidative stress in SD rats with high-salt diet. Hence, H2S inhibited myocardial hypertrophy in high salt-stimulated Dahl rats in association with the enhancement of antioxidant capacity, thereby inhibiting oxidative stress in myocardial tissues.
Highlights
Myocardial hypertrophy is a common cardiovascular pathology, which is an independent risk factor of cardiovascular disease (Cramariuc and Gerdts, 2016)
Compared with rats in Dahl + NS group, H2S content of myocardial tissues was significantly decreased (P < 0.01; Figure 1A) with downregulated CBS mRNA and protein expression (P < 0.01; Figures 1B1,C1) and reduced cystathionine γ-lyase (CSE) mRNA (P < 0.01; Figure 1B2), but CSE protein expression and mercaptopyruvate sulfurtransferase (MPST) mRNA and protein expressions of myocardial tissues did not differ in Dahl + HS group rats (P > 0.05; Figures 1B3,C2,C3)
There was no obvious difference in H2S content and CBS, CSE and MPST mRNA and protein expressions of myocardial tissues among SD + NS group, SD + HS group and SD + HS + NaHS group rats (P > 0.05; Figures 2A–C)
Summary
Myocardial hypertrophy is a common cardiovascular pathology, which is an independent risk factor of cardiovascular disease (Cramariuc and Gerdts, 2016). Our previous studies demonstrated that down-regulation of renal H2S/CBS pathway induced by high salt led to the development of hypertension, and H2S 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 H2S on the function and structure of aorta and kidney participated in the protective regulation of H2S on the myocardial hypertrophy. It is unclear whether endogenous H2S pathway was involved in the pathogenesis of high salt-induced myocardial hypertrophy
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