Document Detail


Hydrogen sulfide attenuates cardiac dysfunction in a rat model of heart failure: a mechanism through cardiac mitochondrial protection.
MedLine Citation:
PMID:  20450490     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
HF (heart failure) after MI (myocardial infarction) is a major cause of morbidity and mortality worldwide. Recent studies have shown that hydrogen sulfide (H2S) has cardioprotective effects. Hence, we aimed to elucidate the potential effects of H2S on HF after MI in rats. The HF model after MI was made by ligating the left anterior descending coronary artery. HF groups and sham-operated groups of rats were treated with vehicle, sodium hydrosulfide (NaHS) or PAG (propagylglycine). Equal volumes of saline, 3.136 mg · kg-1 · day-1 NaHS or 37.5 mg · kg-1 · day-1 PAG, were intraperitoneally injected into rats for 6 weeks after operation. Survival, lung-to-body weight ratio and left ventricular haemodynamic parameters were measured. The protein and gene expression of Bcl-2, Bax, caspase 3 and cytochrome c were analysed by Western blotting and RT-PCR (reverse transcription-PCR). TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling) and EM (electron microscopy) were used to examine apoptosis of heart tissues. NaHS was found to improve the survival and lower the lung-to-body weight ratio. It increased the LVSP (left ventricular systolic pressure) and the maximum rate of pressure and decreased LVEDP (left ventricular end-diastolic pressure). Furthermore, NaHS promoted Bcl-2 protein and mRNA expression and demoted Bax, caspase 3 protein and mRNA expression in HF rats. We also showed that NaHS decreased the leakage of cytochrome c protein from the mitochondria to the cytoplasm. Histological observation by TUNEL and EM proved that NaHS inhibited cardiac apoptosis in HF hearts and improved mitochondrial derangements, but that PAG aggravated those indices. Hence, H2S has protective effects in HF rats.
Authors:
Xianli Wang; Qian Wang; Wei Guo; Yi Zhun Zhu
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Bioscience reports     Volume:  31     ISSN:  1573-4935     ISO Abbreviation:  Biosci. Rep.     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2010-11-24     Completed Date:  2011-03-11     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  8102797     Medline TA:  Biosci Rep     Country:  United States    
Other Details:
Languages:  eng     Pagination:  87-98     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, School of Pharmacy and Institute of Biomedical Sciences, Fudan University, Shanghai, People's Republic of China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects
Blood Pressure / drug effects
Cardiotonic Agents / pharmacology*
Caspase 3 / genetics,  metabolism
Cytochromes c / metabolism
Disease Models, Animal
Gene Expression
Genes, bcl-2
Heart Failure / blood,  drug therapy,  pathology,  physiopathology*
Heart Ventricles / metabolism,  pathology
Hydrogen Sulfide / blood*
Male
Mitochondria, Heart / drug effects,  metabolism*
Mitochondrial Proteins / metabolism
Myocardial Infarction / blood,  drug therapy,  physiopathology
Rats
Sulfides / pharmacology*
Ventricular Function, Left / drug effects
bcl-2-Associated X Protein / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Cardiotonic Agents; 0/Mitochondrial Proteins; 0/Sulfides; 0/bcl-2-Associated X Protein; 7783-06-4/Hydrogen Sulfide; 9007-43-6/Cytochromes c; EC 3.4.22.-/Caspase 3; FWU2KQ177W/sodium bisulfide
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