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The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction

AIM: Rasagiline mesylate (N‐propargyl‐1 (R)‐aminoindan) (RG) is a selective, potent irreversible inhibitor of monoamine oxidase‐B with cardioprotective and anti‐apoptotic properties. We investigated whether it could be cardioprotective in a rat model undergoing experimental myocardial infarction (MI...

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Autores principales: Varela, Aimilia, Mavroidis, Manolis, Katsimpoulas, Michalis, Sfiroera, Irini, Kappa, Niki, Mesa, Angelica, Kostomitsopoulos, Nikolaos G., Cokkinos, Dennis V.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5542732/
https://www.ncbi.nlm.nih.gov/pubmed/28772050
http://dx.doi.org/10.1002/ehf2.12140
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author Varela, Aimilia
Mavroidis, Manolis
Katsimpoulas, Michalis
Sfiroera, Irini
Kappa, Niki
Mesa, Angelica
Kostomitsopoulos, Nikolaos G.
Cokkinos, Dennis V.
author_facet Varela, Aimilia
Mavroidis, Manolis
Katsimpoulas, Michalis
Sfiroera, Irini
Kappa, Niki
Mesa, Angelica
Kostomitsopoulos, Nikolaos G.
Cokkinos, Dennis V.
author_sort Varela, Aimilia
collection PubMed
description AIM: Rasagiline mesylate (N‐propargyl‐1 (R)‐aminoindan) (RG) is a selective, potent irreversible inhibitor of monoamine oxidase‐B with cardioprotective and anti‐apoptotic properties. We investigated whether it could be cardioprotective in a rat model undergoing experimental myocardial infarction (MI) by permanent ligation of the left anterior descending coronary artery. METHODS AND RESULTS: RG was administered, intraperitoneally, for 28 days (2 mg/kg) starting 24 h after MI induction. Echocardiography analysis revealed a significant reduction in left ventricular end‐systolic and diastolic dimensions and preserved fractional shortening in RG‐treated compared with normal saline group at 28 days post‐MI (31.6 ± 2.3 vs. 19.6 ± 1.8, P < 0.0001), respectively. Treatment with RG prevented tissue fibrosis as indicated by interstitial collagen estimation by immunofluorescence staining and hydroxyproline content and attenuated the number of apoptotic myocytes in the border zone (65%) as indicated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Caspase 3 relative protein levels were significantly decreased in the non‐infarcted myocardium. Markedly decreased malondialdehyde levels in the border zone indicate a reduction in tissue oxidative stress. CONCLUSIONS: Our study demonstrates a positive effect of RG in the post‐MI period with a significant attenuation in cardiac remodelling.
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spelling pubmed-55427322017-08-17 The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction Varela, Aimilia Mavroidis, Manolis Katsimpoulas, Michalis Sfiroera, Irini Kappa, Niki Mesa, Angelica Kostomitsopoulos, Nikolaos G. Cokkinos, Dennis V. ESC Heart Fail Original Research Articles AIM: Rasagiline mesylate (N‐propargyl‐1 (R)‐aminoindan) (RG) is a selective, potent irreversible inhibitor of monoamine oxidase‐B with cardioprotective and anti‐apoptotic properties. We investigated whether it could be cardioprotective in a rat model undergoing experimental myocardial infarction (MI) by permanent ligation of the left anterior descending coronary artery. METHODS AND RESULTS: RG was administered, intraperitoneally, for 28 days (2 mg/kg) starting 24 h after MI induction. Echocardiography analysis revealed a significant reduction in left ventricular end‐systolic and diastolic dimensions and preserved fractional shortening in RG‐treated compared with normal saline group at 28 days post‐MI (31.6 ± 2.3 vs. 19.6 ± 1.8, P < 0.0001), respectively. Treatment with RG prevented tissue fibrosis as indicated by interstitial collagen estimation by immunofluorescence staining and hydroxyproline content and attenuated the number of apoptotic myocytes in the border zone (65%) as indicated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Caspase 3 relative protein levels were significantly decreased in the non‐infarcted myocardium. Markedly decreased malondialdehyde levels in the border zone indicate a reduction in tissue oxidative stress. CONCLUSIONS: Our study demonstrates a positive effect of RG in the post‐MI period with a significant attenuation in cardiac remodelling. John Wiley and Sons Inc. 2017-03-12 /pmc/articles/PMC5542732/ /pubmed/28772050 http://dx.doi.org/10.1002/ehf2.12140 Text en © 2017 The Authors ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Research Articles
Varela, Aimilia
Mavroidis, Manolis
Katsimpoulas, Michalis
Sfiroera, Irini
Kappa, Niki
Mesa, Angelica
Kostomitsopoulos, Nikolaos G.
Cokkinos, Dennis V.
The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction
title The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction
title_full The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction
title_fullStr The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction
title_full_unstemmed The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction
title_short The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction
title_sort neuroprotective agent rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction
topic Original Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5542732/
https://www.ncbi.nlm.nih.gov/pubmed/28772050
http://dx.doi.org/10.1002/ehf2.12140
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