Cardiac
mitochondrial dysfunction plays an important role in the pathology of
myocardial infarction. The protective effects of
caffeic acid on
mitochondrial dysfunction in
isoproterenol-induced
myocardial infarction were studied in Wistar rats. Rats were pretreated with
caffeic acid (15 mg/kg) for 10 days. After the pretreatment period,
isoproterenol (100 mg/kg) was subcutaneously injected to rats at an interval of 24 h for 2 days to induce
myocardial infarction.
Isoproterenol-induced rats showed considerable increased levels of serum
troponins and heart mitochondrial lipid peroxidation products and considerable decreased
glutathione peroxidase and
reduced glutathione. Also, considerably decreased activities of
isocitrate,
succinate,
malate, α-ketoglutarate, and
NADH dehydrogenases and
cytochrome-C-oxidase were observed in the mitochondria of myocardial-infarcted rats. The mitochondrial
calcium,
cholesterol,
free fatty acids, and
triglycerides were considerably increased and
adenosine triphosphate and
phospholipids were considerably decreased in
isoproterenol-induced rats.
Caffeic acid pretreatment showed considerable protective effects on all the biochemical parameters studied.
Myocardial infarct size was much reduced in
caffeic acid pretreated
isoproterenol-induced rats. Transmission electron microscopic findings also confirmed the protective effects of
caffeic acid. The possible mechanisms of
caffeic acid on cardiac mitochondria protection might be due to decreasing
free radicals, increasing multienzyme activities,
reduced glutathione, and
adenosine triphosphate levels and maintaining
lipids and
calcium. In vitro studies also confirmed the
free-radical-scavenging activity of
caffeic acid. Thus,
caffeic acid protected rat's heart mitochondria against
isoproterenol-induced damage. This study may have a significant impact on myocardial-infarcted patients.