(-)Epigallocatechingallate protects the mitochondria against the deleterious effects of lipids, calcium and adenosine triphosphate in isoproterenol induced myocardial infarcted male Wistar rats.
The present study was undertaken to evaluate the protective effect of (-)epigallocatechin gallate (EGCG) on mitochondrial lipids, lipid peroxides, Na(+)/K(+) ATPase, calcium and adenosine triphosphate in isoproterenol (ISO) induced myocardial infarction in male Wistar rats. Rats were pretreated with EGCG (30 mg kg(-1) body weight) orally using an intragastric tube daily for a period of 21 days. After that, ISO (100 mg kg(-1) body weight) was subcutaneously injected to rats at intervals of 24 h for two days. ISO induced rats showed significant increase in the levels of cholesterol, triglycerides and free fatty acids with subsequent decrease in the levels of phospholipids in mitochondrial fraction of the heart. ISO induction also caused significant increase in lipid peroxidation products (thiobarbituric acid reactive substances and lipid hydroperoxides) and significant decrease in the activity of Na(+)/K(+) ATPase in mitochondrial fraction of the heart. A significant increase in the levels of calcium and significant decrease in the levels of adenosine triphosphate were observed in ISO-induced mitochondrial heart. Prior treatment with EGCG (30 mg kg(-1)) significantly protected these alterations and maintained normal mitochondrial function. Thus, this study confirmed the protective effect of EGCG on mitochondria in experimentally induced cardiotoxicity in Wistar rats.
Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar 608 002, Tamil Nadu, India.
P T
PT
Devika
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Stanely Mainzen Prince
D000255:Adenosine Triphosphate / Q000037:antagonists & inhibitors / Q000633:toxicity*; D000318:Adrenergic beta-Agonists; D000818:Animals; D002118:Calcium / Q000037:antagonists & inhibitors / Q000633:toxicity*; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002784:Cholesterol / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D007545:Isoproterenol; D008054:Lipid Peroxides / Q000633:toxicity; D008055:Lipids / Q000037:antagonists & inhibitors / Q000633:toxicity*; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects*; D009203:Myocardial Infarction / Q000139:chemically induced* / Q000473:pathology*; D010743:Phospholipids / Q000378:metabolism; D020011:Protective Agents / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism
D000318:Adrenergic beta-Agonists; D005230:Fatty Acids, Nonesterified; D008054:Lipid Peroxides; D008055:Lipids; D010743:Phospholipids; D020011:Protective Agents; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; D000255:Adenosine Triphosphate; D002392:Catechin; D002784:Cholesterol; C045651:epigallocatechin gallate; D000254:Sodium-Potassium-Exchanging ATPase; D007545:Isoproterenol; D002118:Calcium