pharmacology-world-heart-congress-2019-scientifictracks

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Volume 08

Clinical Pharmacology & Biopharmaceutics

ISSN: 2167-065X

Pharmacology 2019

World Heart Congress 2019

August 19-20, 2019

JOINT EVENT

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August 19-20, 2019 Vienna, Austria

World Heart Congress

World Congress on

Pharmacology

MicroRNA 103 inhibitor as a potential promising therapeutic target for myocardial infarction

Ayman Selim, Mai A. Zaafan, Amr M. Abdelhamid, Amr Mohamed Alaa, Bana Ammar, Shahd Yehia, Al Hasnaa Abdel Tawwab, Asmaa Esmail, Heba

Abdelhakim

and

Yara Hamdy

October University for Modern Sciences and Arts (MSA), Egypt

yocardial 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 up-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 sacrificed by cervical dislocation under

urethane anesthesia. Blood and hearts samples were collected for biochemical analysis of miR103, FADD, receptor

interacting protein kinase (RIPK), nuclear factor-kB (NF-kB), tumor necrosis factor-α (TNF-α), interleukine-6 (IL-

6),Troponin-I and creatine kinase-MB (CK-MB). 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 A and B. While miR-103, RIPK, NF-kB, TNF-α and IL-6 showed high levels of expression in group B

that is attenuated in group C. Troponin-I and CK-MB 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.

Ayman Selim et al., Clin Pharmacol Biopharm, Volume 08