Pharmacy - Pharmacology

Myocardial 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.