Mohamed Alaa, AmrSelim Ahmed, AymanAmmar AlBarazi, BanaYehia AlWais, Shahd2019-10-132019-10-132019Copyright © 2019 MSA University. All Rights Reserved.https://t.ly/63XeOMyocardial infarction (MI) is myocardial cell death due to severe and prolonged ischemia produced from atherosclerosis-related coronary artery disease. MI triggers a cascade of events and reparative phases end with myocardial cell necrosis. MicroRNA (miR) is non-coding single stranded RNA that regulates protein expression. miR-103 is used to regulate expression of Fas- associated death domain (FADD) which decreases necroptosis of ischemic myocardium. The study aims to investigate the modulatory effect of regulating mRNAs translation processes of myocardial infarction induced with Isoprenaline HCL 100 mg/kg (ISO) by injecting miR-103 inhibitor. Eighteen mice (15-25 gm) were allocated into three groups; Group A (control) received normal saline, Group B received ISO and Group C received ISO and miR-103 inhibitor. Mice were scarified by cervical dislocation under urethane anesthesia. Blood and hearts samples were collected for biochemical analysis of miR103, FADD, RIPK, IL-6 and Troponin-I. In addition, hearts were used for histopathological examination. Results showed that administration of miR-103 antagomir leads to increase in FADD protein levels in group C compared to group B. While miR-103, RIPK, and IL-6 showed high levels of expression in group B that is attenuated in group C. cardiac troponin-I also supported the previous results. Histopathological test showed normal histological structure in groups A and C while focal degeneration in myocardium in B. Accordingly, these results indicate a promising suppression of MI manifestations upon inhibition of miR-103.enOctober University for Modern Sciences and ArtsUniversity of Modern Sciences and ArtsMSA Universityجامعة أكتوبر للعلوم الحديثة والآدابPharmacologyMyocardial InfarctionOther