Post-Infarct Treatment With [Pyr1]Apelin-13 Exerts Anti-Remodelling and Anti-Apoptotic Effects in Rats' Hearts Publisher Pubmed



Azizi Y¹ ; Imani A² ; Fanaei H^{3, 4} ; Khamse S² ; Parvizi MR⁵ ; Faghihi M²
Source: Kardiologia Polska Published:2017

Abstract

Background: Ischaemic heart disease is the main cause of mortality in the world. After myocardial infarction (MI) cardiomyocytes apoptosis and ventricular remodelling have occurred. Apelin is a peptide that has been shown to exert cardioprotective effects. Aim: The aim of this study was to investigate the anti-apoptotic and anti-remodelling effects of [Pyr1]apelin-13 in the rat model of post-MI. Methods: Thirty-six male Wistar rats were randomly divided into three groups: (1) sham, (2) MI, and (3) MI treated with [Pyr1] apelin-13 (MI+Apel). MI animals were subjected to 30-min ligation of the left anterior descending coronary artery (LAD) and 14 days of reperfusion. Twenty-four hours after LAD ligation, [Pyr1]apelin-13 (10 nmol/kg/day, i.p.) was administered for fve consecutive days. Hypertrophic parameters, left ventricular (LV) remodelling, and gene expression of Apel, apelin receptor (Apelr), Bax, caspase-3 (Casp-3), and Bcl-2 by real-time polymerase chain reaction and cardiomyocytes apoptosis by TUNEL immunostaining were assessed on day 14 post-MI. Results: Post-infarct treatment with [Pyr1]apelin-13 improved myocardial hypertrophic and LV remodelling parameters and led to a signifcant increase in the expression of Apel, Apelr, and Bcl-2, and a decrease in the expression of Bax and Casp-3. Furthermore, treatment with [Pyr1]apelin-13 decreased cardiomyocyte apoptosis. Conclusions: [Pyr1]apelin-13 has anti-hypertrophic, anti-remodelling, and anti-apoptotic effects via overexpression of Apel, Apelr, and Bcl-2 and reduces gene expression of Bax and Casp-3 in the infarcted myocardium, which can in turn lead to repair myocardium. © 2017 Polskie Towarzystwo Kardiologiczne.