Document Detail


Impact of Pycnogenol on cardiac extracellular matrix remodeling induced by L-NAME administration to old mice.
MedLine Citation:
PMID:  17646678     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cardiac remodeling is a determinant of the clinical progression of heart failure and now slowing or reversing remodeling is considered as a potential therapeutic target in heart failure. Pycnogenol has been reported to mediate a number of beneficial effects in the cardiovascular system but its effects on hemodynamic and functional cardiovascular changes following cardiac remodeling have not been elucidated. Therefore, we investigated the influence of Pycnogenol supplementation (30 mg/kg) on left ventricular function and myocardial extracellular matrix composition in old C57BL/6N mice following induction of cardiac remodeling by chronic nitric oxide synthase blockade by NG-nitro-L-arginine methyl ester (L-NAME) administration. L-NAME-treated mice demonstrated dilated cardiomyopathy at compensated state, associated with a significant increase of pro-matrix metalloproteinase (MMP)-9 gene expression and activity, a marked decrease in pro-collagen IIIalpha1 gene expression, and a subsequent reduction in cardiac total and cross-linked collagen content. Upon supplementation with Pycnogenol in L-NAME-exposed mice, cardiac gene expression patterns for pro-MMP-2, -9, and -13, and MMP-9 activity were significantly decreased, associated with a significant increase in cardiac tissue inhibitor of metalloproteinase (TIMP)-4 expression. These findings were coincided with a marked increase in myocardial total and cross-linked collagen content, compared with L-NAME-only-treated mice. Moreover, Pycnogenol treatment was associated with reversal of L-NAME-induced alternations in hemodynamic parameters. These data indicate that Pycnogenol can prevent adverse myocardial remodeling induced by L-NAME, through modulating TIMP and MMPs gene expression, MMPs activity, and further reduction in myocardial collagen degradation rate.
Authors:
Sherma Zibadi; Qianli Yu; Peter J Rohdewald; Douglas F Larson; Ronald Ross Watson
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cardiovascular toxicology     Volume:  7     ISSN:  1530-7905     ISO Abbreviation:  Cardiovasc. Toxicol.     Publication Date:  2007  
Date Detail:
Created Date:  2007-07-24     Completed Date:  2007-10-03     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  101135818     Medline TA:  Cardiovasc Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  10-8     Citation Subset:  IM    
Affiliation:
Nutritional Sciences Department, The University of Arizona, Tucson, AZ, USA.
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MeSH Terms
Descriptor/Qualifier:
Aging / physiology*
Animals
Blood Pressure / drug effects
Collagen / metabolism
Cross-Linking Reagents
Enzyme Inhibitors / toxicity*
Extracellular Matrix / drug effects*
Flavonoids / pharmacology*
Heart / drug effects*
Matrix Metalloproteinases / metabolism
Mice
Mice, Inbred C57BL
Myocardium / cytology
NG-Nitroarginine Methyl Ester / toxicity*
Nitric Oxide Synthase Type III / antagonists & inhibitors*
RNA / biosynthesis,  genetics
Reverse Transcriptase Polymerase Chain Reaction
Ventricular Remodeling / drug effects*
Grant Support
ID/Acronym/Agency:
R01 HL079206-01/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cross-Linking Reagents; 0/Enzyme Inhibitors; 0/Flavonoids; 0/pycnogenols; 50903-99-6/NG-Nitroarginine Methyl Ester; 63231-63-0/RNA; 9007-34-5/Collagen; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 3.4.24.-/Matrix Metalloproteinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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