Caffeic acid protects rat heart mitochondria against isoproterenol-induced oxidative damage.
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.
Kumaran
Kandaswamy Senthil
KS
Department of Biochemistry and Biotechnology, Annamalai University, Annamalai nagar, 608002, Tamil Nadu, India.
Prince
Ponnian Stanely Mainzen
PS
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002109:Caffeic Acids / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D016166:Free Radical Scavengers / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D017665:Hydroxyl Radical / Q000378:metabolism; D007545:Isoproterenol; D007656:Ketoglutaric Acids / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism*; D009203:Myocardial Infarction / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D009245:NADH Dehydrogenase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000378:metabolism; D014336:Troponin / Q000097:blood
D002109:Caffeic Acids; D005230:Fatty Acids, Nonesterified; D016166:Free Radical Scavengers; D007656:Ketoglutaric Acids; D014280:Triglycerides; D014336:Troponin; D017665:Hydroxyl Radical; D000255:Adenosine Triphosphate; D002784:Cholesterol; D005979:Glutathione Peroxidase; D009245:NADH Dehydrogenase; D003576:Electron Transport Complex IV; D005978:Glutathione; D007545:Isoproterenol; D002118:Calcium; C040048:caffeic acid