PURPOSE: 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. CONCLUSION: Edaravone pretreatment reduces the IR-induced lung mitochondrial damage in infant rabbits.
PURPOSE: Free radical scavenger edaravone has been approved as a new drug for treatment of strokepatients. The purpose of this study was to examine whether pretreatment with edaravone could attenuate ischemia-reperfusion (IR)-induced lung damage in infantrabbits. 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. CONCLUSION:Edaravone pretreatment reduces the IR-induced lung mitochondrial damage in infantrabbits.
Authors: Robert D Bongard; Ke Yan; Raymond G Hoffmann; Said H Audi; Xiao Zhang; Brian J Lindemer; Mary I Townsley; Marilyn P Merker Journal: Free Radic Biol Med Date: 2013-08-01 Impact factor: 7.376