title: The protective effect of picroside II against hypoxia/reoxygenation injury in neonatal rat cardiomyocytes.
abstract: BACKGROUND
  Picroside II, an iridoid glucoside found in the root of Picrorhiza scrophulariiflora Pennell (Scrophulariaceae), has been demonstrated to possess potent antioxidant activity. However, whether picroside II has a protective effect against hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury is poorly understood.
  
  
  OBJECTIVE
  To explore the cardioprotective role of picroside II against oxidative stress induced by H/R injury in neonatal rat cardiacmyocytes.
  
  
  METHODS
  The viability and cellular damage of cardiomyocytes were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolim bromide (MTT) and lactate dehydrogenase (LDH) assays, respectively. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), the levels of reduced (GSH) and oxidized glutathione (GSSG), and the contents of malondialdehyde (MDA) were determined by a colorimetric method. The levels of intracellular reactive oxygen species (ROS) and calcium were evaluated by flow cytometric analysis.
  
  
  RESULTS
  We analyzed the effective half-maximal concentration for protection from the dose-response curves and obtained the concentration of 50 µg/mL as EC(50). Pretreated cardiomyocytes with picroside II (50-200 µg/mL), prior to H/R exposure, inhibited LDH activity in culture media and increased cell viability in a dose-dependent manner. This protective effect was accompanied by significantly increasing reduced GSH contents and the activities of SOD and GSH-Px and attenuating MDA and GSSG contents in response to H/R injury. Furthermore, treatment with picroside II also inhibited ROS production and calcium accumulation in cardiomyocytes.
  
  
  CONCLUSIONS
  The present study demonstrates that picroside II protects cardiomyocytes against oxidative-stress injury induced by H/R through reduction of ROS production and calcium accumulation and enhancement of the activity of antioxidant defense.
authors.affiliation: Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, P.R. China. fanjimeng2060@yahoo.cn
authors.forename: Fan-Ji
authors.initials: FJ
authors.lastname: Meng
authors.forename: Zhi-Wen
authors.initials: ZW
authors.lastname: Hou
authors.forename: Yang
authors.initials: Y
authors.lastname: Li
authors.forename: Ying
authors.initials: Y
authors.lastname: Yang
authors.forename: Bo
authors.initials: B
authors.lastname: Yu
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D000975:Antioxidants / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002934:Cinnamates / Q000008:administration & dosage / Q000494:pharmacology*; D003124:Colorimetry; D004305:Dose-Response Relationship, Drug; D005434:Flow Cytometry; D057888:Iridoid Glucosides / Q000008:administration & dosage / Q000494:pharmacology*; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects*; D032261:Picrorhiza / Q000737:chemistry; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D000975:Antioxidants; D002934:Cinnamates; D057888:Iridoid Glucosides; D017382:Reactive Oxygen Species; C416837:picroside II; D002118:Calcium