Abstract
Background: Rosmarinic
acid is a polyphenolic compound with considerable antioxidant activities. We
aimed to investigate its cardioprotective effects against isoproterenol-induced
myocardial infarction (MI) in rats.
Methods: Male
Wistar rats were assigned to 5 groups of control, isoproterenol, and treatments
with 10, 20, 40 mg/kg of rosmarinic acid. Myocardial infarction was induced by
subcutaneous injection of isoproterenol (100 mg/kg) once daily for 2 days.
Rosmarinic acid was injected intraperitoneally once daily for 4 days, from the
day of isoproterenol injection. In the fifth day the animals were anesthetized
and hemodynamic and electrocardiographic parameters were recorded. After
collecting the blood samples, the hearts were removed, weighed immediately to
measure the cardiac enlargement, and kept for further histological studies.
Lactate dehydrogenase and malondialdehyde were measured in the heart tissues
for evaluating the damages and lipid peroxidation, respectively.
Results: Rosmarinic acid
revealed a considerable antioxidant activity in vitro, with IC50 of 6.43µg/ml.
Isoproterenol induced cardiac arrhythmias, myocardial damage and cardiac
enlargement. Rosmarinic acid significantly reduced peripheral neutrophil
percentage and inhibited isoproterenol-induced ST-segment elevation and
R-amplitude depression in the infarcted hearts. It also significantly increased
the mean arterial pressure and heart rate and decreased the left ventricular
end diastolic pressure. The ventricular contractility was considerably improved
by rosmarinic acid. Histopathological evaluations showed that rosmarinic acid
significantly diminished the post-MI necrosis and fibrosis in the myocardium
and inhibited the cardiac edematous.
Conclusion: It is deducible
from the results that rosmarinic acid improves the cardiac performance and
inhibits post-MI myocardial depression, probably due to its anti-oxidative
activity.