title: Cardioprotective effect of salvianolic acid A on isoproterenol-induced myocardial infarction in rats.
abstract: The present study was designed to evaluate the cardioprotective potential of salvianolic acid A on isoproterenol-induced myocardial infarction in rats. Hemodynamic parameters and lead II electrocardiograph were monitored and recorded continuously. Cardiac marker enzymes and antioxidative parameters in serum and heart tissues were measured. Assay for mitochondrial respiratory function and histopathological examination of heart tissues were performed. Isoproterenol-treated rats showed significant increases in the levels of lactate dehydrogenase, aspartate transaminase, creatine kinase and malondialdehyde and significant decreases in the activities of superoxide dismutase, catalase and glutathione peroxidase in serum and heart. These rats also showed declines in left ventricular systolic pressure, maximum and minimum rate of developed left ventricular pressure, and elevation of left ventricular end-diastolic pressure and ST-segment. In addition, mitochondrial respiratory dysfunction characterized by decreased respiratory control ratio and ADP/O was observed in isoproterenol-treated rats. Administration of salvianolic acid A for a period of 8 days significantly attenuated isoproterenol-induced cardiac dysfunction and myocardial injury and improved mitochondrial respiratory function. The protective role of salvianolic acid A against isoproterenol-induced myocardial damage was further confirmed by histopathological examination. The results of our study suggest that salvianolic acid A possessing antioxidant activity has a significant protective effect against isoproterenol-induced myocardial infarction.
authors.affiliation: National Center for Pharmaceutical Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 1 Xian Nong Tan Street, Beijing 100050, PR China.
authors.forename: Shou-bao
authors.initials: SB
authors.lastname: Wang
authors.forename: Shuo
authors.initials: S
authors.lastname: Tian
authors.forename: Fan
authors.initials: F
authors.lastname: Yang
authors.forename: Hai-guang
authors.initials: HG
authors.lastname: Yang
authors.forename: Xiu-ying
authors.initials: XY
authors.lastname: Yang
authors.forename: Guan-hua
authors.initials: GH
authors.lastname: Du
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D001219:Aspartate Aminotransferases / Q000097:blood / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D002109:Caffeic Acids / Q000494:pharmacology* / Q000627:therapeutic use; D002316:Cardiotonic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D002374:Catalase / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood / Q000378:metabolism; D004562:Electrocardiography; D005979:Glutathione Peroxidase / Q000378:metabolism; D006439:Hemodynamics / Q000187:drug effects; D007545:Isoproterenol; D007770:L-Lactate Dehydrogenase / Q000097:blood / Q000378:metabolism; D007773:Lactates / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008929:Mitochondria, Heart / Q000378:metabolism / Q000473:pathology; D009203:Myocardial Infarction / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D002109:Caffeic Acids; D002316:Cardiotonic Agents; D007773:Lactates; D010936:Plant Extracts; D008315:Malondialdehyde; C066201:salvianolic acid A; D007770:L-Lactate Dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase; D007545:Isoproterenol