title: Pretreatment with edaravone reduces lung mitochondrial damage in an infant rabbit ischemia-reperfusion model.
abstract: OBJECTIVE
  Free radical scavenger edaravone has been approved as a new drug for treatment of stroke patients. The purpose of this study was to examine whether pretreatment with edaravone could attenuate ischemia-reperfusion (IR)-induced lung damage in infant rabbits.
  
  
  METHODS
  New Zealand White rabbits (Experimental Animal Center, Nanjing Medical University, Nanjing, China) at age from 15 to 21 days were subjected to sham operation, IR, or edaravone plus IR. Ischemia/reperfusion was induced by clamping the right pulmonary hilum for 1 hour and then removal of the clamp for 4 hours. Edaravone (1 mg/kg, intravenous) was given 5 minutes before ischemia. Concentrations of reactive oxygen species-hydroxyl radical (ROS-HR) and malondialdehyde (MDA), and activities of glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD) in the lung tissue were measured. Mitochondrial membrane potential, swelling rate, and ultrastructure of the lung were analyzed, and histologic condition of the lung was evaluated.
  
  
  RESULTS
  Edaravone pretreatment reduced markedly the productions of ROS-HR and MDA and increased the activities of GSH-PX and SOD. It attenuated both IR-induced decrease in mitochondrial membrane potential from 60% to 14% and IR-induced increase in mitochondrial swelling. As results, the mitochondrial and lung tissue damages were less, leading to an improved survival rate in IR rabbits pretreated with edaravone compared with IR rabbits without the treatment.
  
  
  CONCLUSIONS
  Edaravone pretreatment reduces the IR-induced lung mitochondrial damage in infant rabbits.
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
authors.forename: Wanshan
authors.initials: W
authors.lastname: Qiu
authors.forename: Haiyong
authors.initials: H
authors.lastname: Gu
authors.forename: Liang
authors.initials: L
authors.lastname: Zheng
authors.forename: Jianwei
authors.initials: J
authors.lastname: Zhou
authors.forename: Duan
authors.initials: D
authors.lastname: Chen
authors.forename: Yijiang
authors.initials: Y
authors.lastname: Chen
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology / Q000517:prevention & control*; D000818:Animals; D000833:Animals, Suckling; D000983:Antipyrine / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D003250:Constriction; D004195:Disease Models, Animal; D000077553:Edaravone; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D008168:Lung / Q000098:blood supply / Q000187:drug effects* / Q000473:pathology; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000473:pathology; D008933:Mitochondrial Swelling / Q000187:drug effects; D011292:Premedication; D011817:Rabbits; D011897:Random Allocation; D017382:Reactive Oxygen Species; D015427:Reperfusion Injury / Q000209:etiology / Q000517:prevention & control*; D055397:Ventilator-Induced Lung Injury
chemical_list: D017382:Reactive Oxygen Species; D000077553:Edaravone; D000983:Antipyrine