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Erschienen in: Cardiovascular Drugs and Therapy 3/2013

01.06.2013 | ORIGINAL ARTICLE

Protective Effects of Hydrogen Sulfide Against Chronic Alcohol Intake-Induced Left Ventricular Remodeling in Rats

verfasst von: Xiang Zhou, Xiang Lu, Weiting Xu, Jianchang Chen

Erschienen in: Cardiovascular Drugs and Therapy | Ausgabe 3/2013

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Abstract

Purpose

To investigate the protective effects of hydrogen sulfide (H2S) against chronic alcohol intake-induced left ventricular remodeling and explore the potential mechanisms involved.

Methods

Rats were randomly divided into 4 groups: alcohol group, NaHS group, alcohol + NaHS group, and control group. The echocardiographic and morphometric studies were performed to assess left ventricular remodeling. Oxidative stress was evaluated by detecting MDA, GSH-Px, Tot-SOD, CuZn-SOD and Mn-SOD in the supernatant. Cardiomyocyte apoptotic rate was determined by flow cytometry with Annexin V/PI staining. Western blotting was conducted to detect the expression of Bcl-2 family of apoptosis regulator proteins.

Results

The echocardiographic and morphometric data indicated that H2S has protective effects against chronic alcohol intake-induced left ventricular remodeling. Our findings showed a significant increase in MDA level and decreases in GSH-Px, Tot-SOD, CuZn-SOD and Mn-SOD activities in the alcohol group compared to the control group, while in the alcohol + NaHS group, a significant decrease in MDA level and increases in GSH-Px, Tot-SOD, CuZn-SOD and Mn-SOD activities were found compared to the alcohol group. The apoptotic rate in the alcohol group was significantly higher than in the control group, whereas apoptotic rate in the alcohol + NaHS group was significantly lower than in the alcohol group. In addition, Bcl-2 and Bcl-xL expression was upregulated and Bax expression was downregulated in the alcohol + NaHS group compared to the alcohol group.

Conclusions

Our study demonstrates that H2S protects against chronic alcohol intake-induced left ventricular remodeling via attenuating oxidative stress and apoptosis.
Literatur
1.
Zurück zum Zitat Cohn JN, Ferrari R, Sharpe N. Cardiac remodeling–concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling Behalf of an International Forum on Cardiac Remodeling. J Am Coll Cardiol. 2000;35:569–82.CrossRef Cohn JN, Ferrari R, Sharpe N. Cardiac remodeling–concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling Behalf of an International Forum on Cardiac Remodeling. J Am Coll Cardiol. 2000;35:569–82.CrossRef
2.
Zurück zum Zitat Fernández-Solà J, Lluis M, Sacanella E, Estruch R, Antúnez E, Urbano-Márquez A. Increased myostatin activity and decreased myocyte proliferation in chronic alcoholic cardiomyopathy. Alcohol Clin Exp Res. 2011;35:1220–9.PubMedCrossRef Fernández-Solà J, Lluis M, Sacanella E, Estruch R, Antúnez E, Urbano-Márquez A. Increased myostatin activity and decreased myocyte proliferation in chronic alcoholic cardiomyopathy. Alcohol Clin Exp Res. 2011;35:1220–9.PubMedCrossRef
3.
Zurück zum Zitat Liu W, Li J, Tian W, Xu T, Zhang Z. Chronic alcohol consumption induces cardiac remodeling in mice from Th1 or Th2 background. Exp Mol Pathol. 2011;91:761–7.PubMedCrossRef Liu W, Li J, Tian W, Xu T, Zhang Z. Chronic alcohol consumption induces cardiac remodeling in mice from Th1 or Th2 background. Exp Mol Pathol. 2011;91:761–7.PubMedCrossRef
4.
Zurück zum Zitat Tan Y, Li X, Prabhu SD, et al. Angiotensin II plays a critical role in alcohol-induced cardiac nitrative damage, cell death, remodeling, and cardiomyopathy in a protein kinase C/Nicotinamide adenine dinucleotide phosphate oxidase-dependent manner. J Am Coll Cardiol. 2012;59:1477–86.PubMedCrossRef Tan Y, Li X, Prabhu SD, et al. Angiotensin II plays a critical role in alcohol-induced cardiac nitrative damage, cell death, remodeling, and cardiomyopathy in a protein kinase C/Nicotinamide adenine dinucleotide phosphate oxidase-dependent manner. J Am Coll Cardiol. 2012;59:1477–86.PubMedCrossRef
5.
Zurück zum Zitat Mancardi D, Penna C, Merlino A, Del Soldato P, Wink DA, Pagliaro P. Physiological and pharmacological features of the novel gasotransmitter: hydrogen sulfide. Biochim Biophys Acta. 2009;1787:864–72.PubMedCrossRef Mancardi D, Penna C, Merlino A, Del Soldato P, Wink DA, Pagliaro P. Physiological and pharmacological features of the novel gasotransmitter: hydrogen sulfide. Biochim Biophys Acta. 2009;1787:864–72.PubMedCrossRef
6.
Zurück zum Zitat Wang R. The gasotransmitter role of hydrogen sulfide. Antioxid Redox Signal. 2003;5:493–501.PubMedCrossRef Wang R. The gasotransmitter role of hydrogen sulfide. Antioxid Redox Signal. 2003;5:493–501.PubMedCrossRef
7.
Zurück zum Zitat Moore PK, Bhatia M, Moochhala S. Hydrogen sulfide: from the smell of the past to the mediator of the future? Trends Pharmacol Sci. 2003;24:609–11.PubMedCrossRef Moore PK, Bhatia M, Moochhala S. Hydrogen sulfide: from the smell of the past to the mediator of the future? Trends Pharmacol Sci. 2003;24:609–11.PubMedCrossRef
8.
Zurück zum Zitat Sodha NR, Clements RT, Feng J, et al. The effects of therapeutic sulfide on myocardial apoptosis in response to ischemia-reperfusion injury. Eur J Cardiothorac Surg. 2008;33:906–13.PubMedCrossRef Sodha NR, Clements RT, Feng J, et al. The effects of therapeutic sulfide on myocardial apoptosis in response to ischemia-reperfusion injury. Eur J Cardiothorac Surg. 2008;33:906–13.PubMedCrossRef
9.
Zurück zum Zitat Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American society of echocardiography committee on standards, subcommittee on quantitation of two-dimensional echocardiograms. J Am Soc Echocardiogr. 1989;2:358–67.PubMed Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American society of echocardiography committee on standards, subcommittee on quantitation of two-dimensional echocardiograms. J Am Soc Echocardiogr. 1989;2:358–67.PubMed
10.
Zurück zum Zitat Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 1976;72:248–54.PubMedCrossRef Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 1976;72:248–54.PubMedCrossRef
11.
Zurück zum Zitat Laonigro I, Correale M, Di Biase M, Altomare E. Alcohol abuse and heart failure. Eur J Heart Fail. 2009;11:453–62.PubMedCrossRef Laonigro I, Correale M, Di Biase M, Altomare E. Alcohol abuse and heart failure. Eur J Heart Fail. 2009;11:453–62.PubMedCrossRef
12.
Zurück zum Zitat Bian JS, Yong QC, Pan TT, et al. Role of hydrogen sulfide in the cardioprotection caused by ischemic preconditioning in the rat heart and cardiac myocytes. J Pharmacol Exp Ther. 2006;316:670–8.PubMedCrossRef Bian JS, Yong QC, Pan TT, et al. Role of hydrogen sulfide in the cardioprotection caused by ischemic preconditioning in the rat heart and cardiac myocytes. J Pharmacol Exp Ther. 2006;316:670–8.PubMedCrossRef
13.
Zurück zum Zitat Elrod JW, Calvert JW, Morrison J, et al. Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function. Proc Natl Acad Sci U S A. 2007;104:15560–5.PubMedCrossRef Elrod JW, Calvert JW, Morrison J, et al. Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function. Proc Natl Acad Sci U S A. 2007;104:15560–5.PubMedCrossRef
14.
Zurück zum Zitat Hori M, Nishida K. Oxidative stress and left ventricular remodelling after myocardial infarction. Cardiovasc Res. 2009;81:457–64.PubMedCrossRef Hori M, Nishida K. Oxidative stress and left ventricular remodelling after myocardial infarction. Cardiovasc Res. 2009;81:457–64.PubMedCrossRef
15.
Zurück zum Zitat Kameda K, Matsunaga T, Abe N, et al. Correlation of oxidative stress with activity of matrix metalloproteinase in patients with coronary artery disease. Possible role for left ventricular remodelling. Eur Heart J. 2003;24:2180–5.PubMedCrossRef Kameda K, Matsunaga T, Abe N, et al. Correlation of oxidative stress with activity of matrix metalloproteinase in patients with coronary artery disease. Possible role for left ventricular remodelling. Eur Heart J. 2003;24:2180–5.PubMedCrossRef
16.
Zurück zum Zitat Lord KC, Shenouda SK, McIlwain E, Charalampidis D, Lucchesi PA, Varner KJ. Oxidative stress contributes to methamphetamine-induced left ventricular dysfunction. Cardiovasc Res. 2010;87:111–8.PubMedCrossRef Lord KC, Shenouda SK, McIlwain E, Charalampidis D, Lucchesi PA, Varner KJ. Oxidative stress contributes to methamphetamine-induced left ventricular dysfunction. Cardiovasc Res. 2010;87:111–8.PubMedCrossRef
17.
Zurück zum Zitat Murdoch CE, Zhang M, Cave AC, Shah AM. NADPH oxidasedependent redox signalling in cardiac hypertrophy, remodelling and failure. Cardiovasc Res. 2006;71:208–15.PubMedCrossRef Murdoch CE, Zhang M, Cave AC, Shah AM. NADPH oxidasedependent redox signalling in cardiac hypertrophy, remodelling and failure. Cardiovasc Res. 2006;71:208–15.PubMedCrossRef
18.
Zurück zum Zitat Sawyer DB, Siwik DA, Xiao L, Pimentel DR, Singh K, Colucci WS. Role of oxidative stress in myocardial hypertrophy and failure. J Mol Cell Cardiol. 2002;34:379–88.PubMedCrossRef Sawyer DB, Siwik DA, Xiao L, Pimentel DR, Singh K, Colucci WS. Role of oxidative stress in myocardial hypertrophy and failure. J Mol Cell Cardiol. 2002;34:379–88.PubMedCrossRef
19.
Zurück zum Zitat Giordano FJ. Oxygen, oxidative stress, hypoxia, and heart failure. J Clin Invest. 2005;115:500–8.PubMed Giordano FJ. Oxygen, oxidative stress, hypoxia, and heart failure. J Clin Invest. 2005;115:500–8.PubMed
20.
Zurück zum Zitat Zima AV, Blatter LA. Redox regulation of cardiac calcium channels and transporters. Cardiovasc Res. 2006;71:310–21.PubMedCrossRef Zima AV, Blatter LA. Redox regulation of cardiac calcium channels and transporters. Cardiovasc Res. 2006;71:310–21.PubMedCrossRef
21.
Zurück zum Zitat Sabri A, Hughie HH, Lucchesi PA. Regulation of hypertrophic and apoptotic signaling pathways by reactive oxygen species in cardiac myocytes. Antioxid Redox Signal. 2003;5:731–40.PubMedCrossRef Sabri A, Hughie HH, Lucchesi PA. Regulation of hypertrophic and apoptotic signaling pathways by reactive oxygen species in cardiac myocytes. Antioxid Redox Signal. 2003;5:731–40.PubMedCrossRef
22.
Zurück zum Zitat Cheng TH, Cheng PY, Shih NL, Chen IB, Wang DL, Chen JJ. Involvement of reactive oxygen species in angiotensin II-induced endothelin-1 gene expression in rat cardiac fibroblasts. J Am Coll Cardiol. 2003;42:1845–54.PubMedCrossRef Cheng TH, Cheng PY, Shih NL, Chen IB, Wang DL, Chen JJ. Involvement of reactive oxygen species in angiotensin II-induced endothelin-1 gene expression in rat cardiac fibroblasts. J Am Coll Cardiol. 2003;42:1845–54.PubMedCrossRef
23.
Zurück zum Zitat Siwik DA, Pagano PJ, Colucci WS. Oxidative stress regulates collagen synthesis and matrix metalloproteinase activity in cardiac fibroblasts. Am J Physiol Cell Physiol. 2001;280:C53–60.PubMed Siwik DA, Pagano PJ, Colucci WS. Oxidative stress regulates collagen synthesis and matrix metalloproteinase activity in cardiac fibroblasts. Am J Physiol Cell Physiol. 2001;280:C53–60.PubMed
24.
Zurück zum Zitat Kimura Y, Kimura H. Hydrogen sulfide protects neurons from oxidative stress. FASEB J. 2004;18:1165–7.PubMed Kimura Y, Kimura H. Hydrogen sulfide protects neurons from oxidative stress. FASEB J. 2004;18:1165–7.PubMed
25.
Zurück zum Zitat Calvert JW, Jha S, Gundewar S, et al. Hydrogen sulfide mediates cardioprotection through Nrf2 signaling. Circ Res. 2009;105:365–74.PubMedCrossRef Calvert JW, Jha S, Gundewar S, et al. Hydrogen sulfide mediates cardioprotection through Nrf2 signaling. Circ Res. 2009;105:365–74.PubMedCrossRef
26.
Zurück zum Zitat Chandrashekhar Y. Role of apoptosis in ventricular remodeling. Curr Heart Fail Rep. 2005;2:18–22.PubMedCrossRef Chandrashekhar Y. Role of apoptosis in ventricular remodeling. Curr Heart Fail Rep. 2005;2:18–22.PubMedCrossRef
27.
Zurück zum Zitat Abbate A, Biondi-Zoccai GG, Baldi A. Pathophysiologic role of myocardial apoptosis in post-infarction left ventricular remodeling. J Cell Physiol. 2002;193:145–53.PubMedCrossRef Abbate A, Biondi-Zoccai GG, Baldi A. Pathophysiologic role of myocardial apoptosis in post-infarction left ventricular remodeling. J Cell Physiol. 2002;193:145–53.PubMedCrossRef
28.
Zurück zum Zitat Ibe W, Saraste A, Lindemann S, et al. Cardiomyocyte apoptosis is related to left ventricular dysfunction and remodelling in dilated cardiomyopathy, but is not affected by growth hormone treatment. Eur J Heart Fail. 2007;9:160–7.PubMedCrossRef Ibe W, Saraste A, Lindemann S, et al. Cardiomyocyte apoptosis is related to left ventricular dysfunction and remodelling in dilated cardiomyopathy, but is not affected by growth hormone treatment. Eur J Heart Fail. 2007;9:160–7.PubMedCrossRef
29.
Zurück zum Zitat Abbate A, Biondi-Zoccai GG, Bussani R, et al. Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure. J Am Coll Cardiol. 2003;41:753–60.PubMedCrossRef Abbate A, Biondi-Zoccai GG, Bussani R, et al. Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure. J Am Coll Cardiol. 2003;41:753–60.PubMedCrossRef
30.
Zurück zum Zitat Hu Y, Chen X, Pan TT, et al. Cardioprotection induced by hydrogen sulfide preconditioning involves activation of ERK and PI3K/Akt pathways. Pflugers Arch. 2008;455:607–16.PubMedCrossRef Hu Y, Chen X, Pan TT, et al. Cardioprotection induced by hydrogen sulfide preconditioning involves activation of ERK and PI3K/Akt pathways. Pflugers Arch. 2008;455:607–16.PubMedCrossRef
31.
Zurück zum Zitat Yong QC, Lee SW, Foo CS, Neo KL, Chen X, Bian JS. Endogenous hydrogen sulphide mediates the cardioprotection induced by ischemic postconditioning. Am J Physiol Heart Circ Physiol. 2008;295:H1330–40.PubMedCrossRef Yong QC, Lee SW, Foo CS, Neo KL, Chen X, Bian JS. Endogenous hydrogen sulphide mediates the cardioprotection induced by ischemic postconditioning. Am J Physiol Heart Circ Physiol. 2008;295:H1330–40.PubMedCrossRef
Metadaten
Titel
Protective Effects of Hydrogen Sulfide Against Chronic Alcohol Intake-Induced Left Ventricular Remodeling in Rats
verfasst von
Xiang Zhou
Xiang Lu
Weiting Xu
Jianchang Chen
Publikationsdatum
01.06.2013
Verlag
Springer US
Erschienen in
Cardiovascular Drugs and Therapy / Ausgabe 3/2013
Print ISSN: 0920-3206
Elektronische ISSN: 1573-7241
DOI
https://doi.org/10.1007/s10557-013-6441-5

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