title: Investigation of therapeutic potential and molecular mechanism of vitamin P and digoxin in I/R-induced myocardial infarction in rat.
abstract: Ischemic-reperfusion (I/R) is a major event in the pathogenesis of ischemic heart disease that leads to higher rate of mortality. The study has been designed to investigate the therapeutic potential and molecular mechanism of vitamin P and digoxin in I/R-induced myocardial infarction in isolated rat heart preparation by using Langendorff apparatus. The animals were treated with vitamin P (50 and 100 mg/kg; p.o.) and digoxin (500 μg/kg) for 5 consecutive days. Digoxin served as a positive control in the present study. On the sixth day, the heart was harvested and induced to 30 min of global ischemia followed by 120 min of reperfusion using Langendorff apparatus. The coronary effluent was collected at different time intervals (i.e. basal, 1, 15, 30, 45, 60 and 120 min.) for the assessment of myocardial contractility function. In addition, creatine kinase-M and B subunits (CK-MB), lactate dehydrogenase (LDH1) and Na(+)-K(+)-ATPase activity along with oxidative tissue biomarkers (i.e. thio-barbituric acid reactive substances (TBARS) and reduced glutathione (GSH)) changes were estimated. The I/R of myocardium produced decrease in coronary flow rate; increase in CK-MB, LDH1 and Na(+)-K(+)-ATPase activity along with increase in TBARS and decrease in GSH levels as compared to normal group. The treatment with vitamin P (100 mg/kg) and digoxin (500 μg/kg) have produced a significant (p < 0.05) ameliorative effect against I/R induced above functional, metabolic and tissue biomarkers changes. Vitamin P has an ameliorative potential against I/R induced myocardial functional changes. It may be due to its free radical scavenging and anti-infarct property via inhibition of Na(+)-K(+)-ATPase activity. Therefore, it can be used as a potential therapeutic medicine for the management of cardiovascular disorders.
authors.affiliation: Department of Pharmacology, Cardiovascular Division, Akal Toxicology Research Centre, Akal College of Pharmacy and Technical Education, Mastuana Sahib, Sangrur, 148001, Punjab, India.
authors.forename: Harwinder
authors.initials: H
authors.lastname: Singh
authors.forename: Parneet
authors.initials: P
authors.lastname: Kaur
authors.forename: Pradeep
authors.initials: P
authors.lastname: Kaur
authors.forename: Arunachalam
authors.initials: A
authors.lastname: Muthuraman
authors.forename: Gurpreet
authors.initials: G
authors.lastname: Singh
authors.forename: Manjinder
authors.initials: M
authors.lastname: Kaur
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D003326:Coronary Circulation / Q000187:drug effects; D004077:Digoxin / Q000008:administration & dosage / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D000067268:Isolated Heart Preparation; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000150:complications* / Q000503:physiopathology; D018384:Oxidative Stress / Q000187:drug effects; D017207:Rats, Sprague-Dawley; D012431:Rutin / Q000008:administration & dosage / Q000627:therapeutic use*
chemical_list: D002316:Cardiotonic Agents; D012431:Rutin; D004077:Digoxin