The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction. (12th March 2017)

• Record Type: Journal Article
• Authors: Varela, Aimilia; Mavroidis, Manolis; Katsimpoulas, Michalis; Sfiroera, Irini; Kappa, Niki; Mesa, Angelica; Kostomitsopoulos, Nikolaos G.; Cokkinos, Dennis V.
• Is Part Of: ESC heart failure. Volume 4:Number 3(2017)
• Page Start: 331
• Page End: 340
• Publication Date: 2017-03-12
• Subjects: Rasagiline mesylate -- Myocardial infarction -- Cardiac remodelling -- Fibrosis -- Apoptosis; Heart failure -- Periodicals; 616.129005
• DOI: 10.1002/ehf2.12140
• Languages: English
• ISSNs: 2055-5822

Abstract

Abstract: 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.