Document Detail

Protective effects of hydroxysafflor yellow A on acute and chronic congestive cardiac failure mediated by reducing ET-1, NOS and oxidative stress in rats.
MedLine Citation:
PMID:  18088512     Owner:  NLM     Status:  MEDLINE    
The present study was conducted to investigate whether hydroxysafflor yellow A (HSYA) has a protective effect on acute and chronic heart failure (AHF/CHF) induced by ligation of the left anterior descending coronary artery for 3 h and 8 weeks, respectively. The rats were divided into the following groups: sham operation, coronary artery ligation (CAL), CAL+HSYA (100 mg kg(-1) by gavage) and CAL+diltiazem (20 mg kg(-1) by gavage). In the AHF model, heart function, as determined by haemodynamic studies and echocardiography, was improved significantly by pretreatment with HSYA or diltiazem. Significant reductions in elevated serum creatine phosphokinase, lactate dehydrogenase, malondialdehyde (MDA), glutamic oxalacetic transaminase, glutamic pyruvic transaminase and blood viscosity were observed, and the activity of serum superoxide dismutase (SOD) was enhanced (all P<0.01). In the CHF model, HSYA and diltiazem restored abnormal heart function, and completely suppressed the elevated plasma atrial natriuretic polypeptide (ANP) and endothelin-1 (ET-1), serum and left-ventricular tissue inducible nitric oxide (NO) synthase (iNOS), NO and MDA, and improved the decrease in SOD. HSYA and diltiazem improved cardiac performance in AHF and reduced cardiac remodelling in CHF by reducing tissue weight indices: left ventricular weight/body weight (BW), right ventricular weight/BW, kidney weight/BW and lung weight/BW, and attenuating increases in infarct size, inner diameter of the left ventricle and collagen volume fraction in non-infarcted areas, and the decrease in mean wall thickness of infarcted myocardium. These results suggest that HSYA exerted beneficial actions in cardiac performance in models of both AHF and CHF, mainly by suppressing ET-1, iNOS and oxidative stress in infarcted tissue.
Haibo He; Xianzhe Yang; Mengqiong Shi; Xiaowei Zeng; Jun Yang; Limao Wu; Lianda Li
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication    
Journal Detail:
Title:  The Journal of pharmacy and pharmacology     Volume:  60     ISSN:  0022-3573     ISO Abbreviation:  J. Pharm. Pharmacol.     Publication Date:  2008 Jan 
Date Detail:
Created Date:  2007-12-19     Completed Date:  2008-05-12     Revised Date:  2009-08-20    
Medline Journal Info:
Nlm Unique ID:  0376363     Medline TA:  J Pharm Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  115-23     Citation Subset:  IM    
Institute of Chinese Herb Medicine, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang, 310058, P. R. China.
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MeSH Terms
Acute Disease
Alanine Transaminase / blood
Aspartate Aminotransferases / blood
Blood Viscosity / drug effects
Cardiotonic Agents / pharmacology*,  therapeutic use
Chalcone / analogs & derivatives*,  pharmacology,  therapeutic use
Chronic Disease
Coronary Vessels / surgery
Creatine Kinase / blood
Diltiazem / pharmacology,  therapeutic use
Disease Models, Animal
Echocardiography / methods
Endothelin-1 / blood*
Heart Failure / blood,  drug therapy*,  etiology
Hemodynamics / drug effects
L-Lactate Dehydrogenase / blood
Ligation / adverse effects
Malondialdehyde / blood
Nitric Oxide Synthase / blood*
Oxidative Stress / drug effects*
Quinones / pharmacology*,  therapeutic use
Rats, Sprague-Dawley
Superoxide Dismutase / blood
Reg. No./Substance:
0/Cardiotonic Agents; 0/Endothelin-1; 0/Quinones; 146087-19-6/hydroxysafflor yellow A; 42399-41-7/Diltiazem; 542-78-9/Malondialdehyde; 94-41-7/Chalcone; EC Dehydrogenase; EC Oxide Synthase; EC Dismutase; EC Aminotransferases; EC Transaminase; EC Kinase
Retraction In:
Jones DS. J Pharm Pharmacol. 2009 May;61(5):685   [PMID:  19406009 ]

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