Hydrogen sulfide attenuates cardiac hypertrophy and fibrosis induced by abdominal aortic coarctation in rats

Department of Cardiology, Medical College, The First Affiliated Hospital of Shantou University, Shantou, Guangdong 515041, PR China.
Molecular Medicine Reports (Impact Factor: 1.55). 04/2012; 5(4):923-8. DOI: 10.3892/mmr.2012.748
Source: PubMed


Hydrogen sulfide (H2S) has been recently found to be an endogenous signaling gasotransmitter. Cardiac hypertrophy often develops in the course of heart failure. It is unknown whether or not endogenous H2S protects cardiac hypertrophy. This study was conducted to examine the effects of H2S on cardiac hypertrophy and fibrosis induced by abdominal aortic coarctation and to explore its mechanisms. Male Sprague-Dawley rats were randomly divided into five groups: normal, sham, abdominal aortic coarctation (AAC), AAC treated with enalapril and AAC treated with H2S. One week after surgery, enalapril and sodium hydrosulfide (NaHS)-treated rats were fed for 28 consecutive days and sacrificed. After that, the left ventricle mass index (LVMI), cardiomyocyte size and areas, collagen volume fraction (CVF) of the rats were measured. In the AAC rats, the LVMI, the cardiomyocyte size and areas, and the CVF were all markedly increased while in the H2S groups they were significantly reduced. H2S decreased the levels of Ang-II in the heart, but not in plasma. In addition, H2S also improved the expression of connexin 43 (Cx43). Our results suggest that H2S can significantly suppress cardiac hypertrophy and fibrosis induced by overloaded pressure, possibly by inhibiting the activity of intracardiac Ang-II and by modifying expression of Cx43.

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Available from: Hong Jin, Aug 05, 2014
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    • "Mishra et al. [49] found cardiac fibrosis and apoptosis in chronic heart failure (CHF) were reversed by administration of H 2 S, which was associated with a decrease in oxidative and proteolytic stresses. In addition, Huang et al. [45] revealed that H 2 S markedly prevented the development of cardiac fibrosis and decreased the collagen content in the cardiac tissue by inhibiting the activity of intracardiac Ang-II. It is well known that multiple potassium channels are expressed in cardiac ventricular fibroblasts [50], whereby their modulations may have major significance in cardiac fibrosis. "
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    ABSTRACT: Hydrogen sulfide (H2S) is now recognized as a third gaseous mediator along with nitric oxide (NO) and carbon monoxide (CO), though it was originally considered as a malodorous and toxic gas. H2S is produced endogenously from cysteine by three enzymes in mammalian tissues. An increasing body of evidence suggests the involvement of H2S in different physiological and pathological processes. Recent studies have shown that H2S has the potential to protect the heart against myocardial infarction, arrhythmia, hypertrophy, fibrosis, ischemia-reperfusion injury, and heart failure. Some mechanisms, such as antioxidative action, preservation of mitochondrial function, reduction of apoptosis, anti-inflammatory responses, angiogenic actions, regulation of ion channel, and interaction with NO, could be responsible for the cardioprotective effect of H2S. Although several mechanisms have been identified, there is a need for further research to identify the specific molecular mechanism of cardioprotection in different cardiac diseases. Therefore, insight into the molecular mechanisms underlying H2S action in the heart may promote the understanding of pathophysiology of cardiac diseases and lead to new therapeutic targets based on modulation of H2S production.
    Oxidative medicine and cellular longevity 06/2015; 2015:1-13. DOI:10.1155/2015/925167 · 3.36 Impact Factor
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    • "Downregulation of CBS and CSE expression/activity and decreased plasma H 2 S levels were observed in patients with hepatocirrhosis [20] [21] [22] [23]. And animal models of various organ fibrosis demonstrated the significant decrease of the endogenous H 2 S level in plasma and tissues and the H 2 S-producing enzymes, whereas the administration exogenous H 2 S could inhibit the fibrosis development [9] [13] [15] [18] [19] [24] [25]. "
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    ABSTRACT: Hydrogen sulfide (H2S), produced endogenously by the activation of two major H2S-generating enzymes (cystathionine β-synthase and cystathionine γ-lyase), plays important regulatory roles in different physiologic and pathologic conditions. The abnormal metabolism of H2S is associated with fibrosis pathogenesis, causing damage in structure and function of different organs. A number of in vivo and in vitro studies have shown that both endogenous H2S level and the expressions of H2S-generating enzymes in plasma and tissues are significantly downregulated during fibrosis. Supplement with exogenous H2S mitigates the severity of fibrosis in various experimental animal models. The protective role of H2S in the development of fibrosis is primarily attributed to its antioxidation, antiapoptosis, anti-inflammation, proangiogenesis, and inhibition of fibroblasts activities. Future studies might focus on the potential to intervene fibrosis by targeting the pathway of endogenous H2S-producing enzymes and H2S itself.
    Oxidative medicine and cellular longevity 06/2015; 2015:1-12. DOI:10.1155/2015/593407 · 3.36 Impact Factor

  • Journal of cardiac failure 08/2012; 18(8):597-9. DOI:10.1016/j.cardfail.2012.06.414 · 3.05 Impact Factor
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