CONDUCTED BY: Laboratory of Animal Physiology, Faculty of Sciences of Sfax, University of Sfax, Sfax, Tunisia; Department of Internal Medicine, Hospital of Sidi Bouzid,TunisiA; Laboratory of Chemistry of Natural Products, Faculty of Sciences of Sfax, University of Sfax, Sfax, Tunisia; Faculty of Medicine of Monastir, Avenue Avicenne, Monastir, Tunisia; Department of Cardiology, Centre Hospitalier Intercommunal Robert Ballanger, Aulnay-Sous-Bois, France; Laboratory of Plant Biotechnology, Faculty of Sciences of Sfax, University of Sfax,Tunisia
PUBLISHED ON: Cardiovascular Toxicology
The present study aimed to investigate the cardioprotective effect of hydroxytyrosol (HT) against isoproterenol-induced myocardial infarction in rats. Male rats were randomly divided into four groups, control, isoproterenol (Isop) and pretreated animals with HT in two different doses (2 and 5 mg/kg) orally for 7 days and intoxicated with isoproterenol (Isop + HT1) and (Isop + HT2) groups.
Myocardial infarction in rats was induced subcutaneously by isoproterenol (100 mg/kg, s.c.) at an interval of 24h on 6th and 7th day. On 8th day, electrocardiographic (ECG) pattern, gravimetric and biochemical parameters were assessed. Isoproterenol exhibited changes in ECG pattern, including significant ST-segment elevation and increase in the serum troponin-T level by 317% as compared to control rats.
Moreover, cardiac injury markers (creatine kinase-MB, lactate dehydrogenase, alanine aminotransferase) underwent a notable rise in serum of infarcted animals. Else, a disturbance in lipids profile and significant increase in lipase and angiotensin-converting enzyme (ACE) activities and heart weight ratio were observed in isoproterenol group. However, pre- and co-treatment with hydroxytyrosol (2 and 5mg/kg) improved the myocardium injury, restored the hemodynamic function and inhibited the ACE activity that prevent cardiac hypertrophy and remodeling.
Overall, these findings demonstrated that hydroxytyrosol exerted a potent cardioprotective effect against isoproterenol-induced myocardial infarction.