Document Detail


Prevention of myocardial fibrosis by N-acetyl-seryl-aspartyl-lysyl-proline in diabetic rats.
MedLine Citation:
PMID:  20310083     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline) is a physiological tetrapeptide hydrolysed by ACE (angiotensin-converting enzyme). In experimental models of hypertension, Ac-SDKP has antifibrotic effects in the heart; however, the role of Ac-SDKP in diabetic cardiomyopathy is currently unknown. The aim of the present study was to evaluate the effect of Ac-SDKP on cardiac systolic and diastolic function, and interstitial and perivascular fibrosis in the heart of diabetic rats.Diabetes was induced in 55 Sprague-Dawley rats by streptozotocin injection. Control rats (n=18)underwent only buffer injection.Out of the 55 diabetic rats, 19 were chronically treated with insulin and 13 with the ACEI (ACE inhibitor) ramipril (3 mg x kg(-1 )of body weight x day(-1)). At 2 months after the onset of diabetes, Ac-SDKP (1 mg x kg(-1) of body weight x day(-1)) was administered by osmotic minipumps for 8 weeks to eight control rats, 13 diabetic rats, seven diabetic rats treated with ramipril and nine insulin-treated diabetic rats. Diabetic rats had a significant increase in blood glucose levels. Left ventricular interstitial and perivascular fibrosis, and TGF-beta1 (transforming growth factor-beta1) protein levels were increased in diabetic rats, but not in insulin-treated diabetic rats and ramipril-treated diabetic rats, compared with control rats. Ac-SDKP administration significantly reduced left ventricular interstitial and perivascular fibrosis in diabetic rats and in diabetic rats treated with ramipril. This was accompanied by a significant reduction in active TGF-beta1 and phospho-Smad2/3 protein levels in myocardial tissue of diabetic rats. Echocardiography showed that diabetes was associated with increased end-systolic diameters, and depressed global systolic function and diastolic dysfunction, as assessed by transmitral Doppler velocity profile. These changes were completely reversed by insulin or ramipril treatment. Ac-SDKP treatment partially restored diastolic function in diabetic rats. In conclusion, Ac-SDKP administration in diabetic rats reduces left ventricular interstitial and perivascular fibrosis, active TGF-beta1 and phospho-Smad2/3levels, and improves diastolic function. Taken together, these findings suggest that, by inhibiting theTGF-beta/Smad pathway, Ac-SDKP protects against the development of diabetic cardiomyopathy
Authors:
Giovanna Castoldi; Cira R T di Gioia; Camila Bombardi; Carla Perego; Lucia Perego; Massimiliano Mancini; Martina Leopizzi; Barbara Corradi; Stefano Perlini; Gianpaolo Zerbini; Andrea Stella
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Publication Detail:
Type:  Journal Article     Date:  2009-10-26
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  118     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-03-22     Completed Date:  2010-03-25     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  211-20     Citation Subset:  IM    
Affiliation:
Clinica Nefrologica, Az Ospedaliera San Gerardo, 20052 Monza, Italy. giovanna.castoldi@unimib.it
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MeSH Terms
Descriptor/Qualifier:
Angiotensin-Converting Enzyme Inhibitors / administration & dosage
Animals
Cardiomyopathies / prevention & control
Diabetes Complications / prevention & control*
Diabetes Mellitus, Experimental / physiopathology*
Fibrosis
Heart Ventricles / drug effects,  pathology*
Hypoglycemic Agents / administration & dosage
Insulin / administration & dosage
Male
Myocardium / pathology*
Oligopeptides / administration & dosage,  pharmacology*
Ramipril / administration & dosage
Rats
Rats, Sprague-Dawley
Smad Proteins / drug effects,  metabolism
Transforming Growth Factor beta1 / drug effects,  metabolism
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Hypoglycemic Agents; 0/Oligopeptides; 0/Smad Proteins; 0/Transforming Growth Factor beta1; 11061-68-0/Insulin; 120081-14-3/goralatide; 87333-19-5/Ramipril

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


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