Cromakalin pretreatment affects mitochondrial structure and function in a rat model of ischemia/reperfusion injury  被引量:6

Cromakalin pretreatment affects mitochondrial structure and function in a rat model of ischemia/reperfusion injury

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作  者:Shilei Wang Peng Wang Qingxian Chang Yu Li Yan Jiang Shiduan Wang 

机构地区:[1]Department of Anesthesiology, Affiliated Hospital of Qingdao University Medical College, Qingdao 266003, Shandong Province, China

出  处:《Neural Regeneration Research》2008年第9期933-938,共6页中国神经再生研究(英文版)

摘  要:BACKGROUND:Mitochondrial structural changes and energy dysmetabolism frequently occur subsequent to cerebral ischemia.Adenosine triphosphate(ATP)-sensitive potassium channel openers exhibit protective effects on cerebral ischemia/reperfusion injury.OBJECTIVE:To validate the effects of cromakalin on mitochondrial structure and function in ischemic penumbra brain tissue in a rat model of middle cerebral artery occlusion(MCAO).DESIGN,TIME AND SETTING:The present single-factor analysis of variance,randomized,controlled,animal experiment was performed at the Institute of Brain Science,Affiliated Hospital of Qingdao University Medical College between October 2007 and March 2008.MATERIALS:Forty male,Wistar rats were randomly divided into four groups,with 10 rats per group:sham-operated,MCAO,MCAO+ATP-sensitive potassium channel opener(cromakalin),and MCAO+cromakalin+ATP-sensitive potassium channel blocking agent(glibenclamide).METHODS:Focal cerebral ischemia/reperfusion injury was induced by MCAO in all groups except the sham-operated group.The MCAO cromakalin group was administered 10 mg/kg cromakalin(i.p.) prior to MCAO induction.The MCAO+cromakalin+glibenclamide group received an injection of 10 mg/kg cromakalin(i.v.),and subsequently an injection of 10 mg/kg cromakalin(i.p.) prior to MCAO induction.MAIN OUTCOME MEASURES:At 24 hours after cerebral ischemia/reperfusion injury,cellular apoptosis was detected by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate(dUTP) nick-end labeling technique.Cytochrome C expression was measured by immunohistochemistry.In addition,mitochondrial swelling,membrane fluidity,membrane phospholipid and malonaldehyde(MDA) contents,as well as Na^+-K^+-ATPase,Ca^2 +-ATPase,and superoxide dismutase(SOD) activities were determined.RESULTS:Compared with the sham-operated group,the three ischemia groups exhibited significantly elevated mitochondrial MDA content,reduced membrane phospholipid and ATP contenBACKGROUND:Mitochondrial structural changes and energy dysmetabolism frequently occur subsequent to cerebral ischemia.Adenosine triphosphate(ATP)-sensitive potassium channel openers exhibit protective effects on cerebral ischemia/reperfusion injury.OBJECTIVE:To validate the effects of cromakalin on mitochondrial structure and function in ischemic penumbra brain tissue in a rat model of middle cerebral artery occlusion(MCAO).DESIGN,TIME AND SETTING:The present single-factor analysis of variance,randomized,controlled,animal experiment was performed at the Institute of Brain Science,Affiliated Hospital of Qingdao University Medical College between October 2007 and March 2008.MATERIALS:Forty male,Wistar rats were randomly divided into four groups,with 10 rats per group:sham-operated,MCAO,MCAO+ATP-sensitive potassium channel opener(cromakalin),and MCAO+cromakalin+ATP-sensitive potassium channel blocking agent(glibenclamide).METHODS:Focal cerebral ischemia/reperfusion injury was induced by MCAO in all groups except the sham-operated group.The MCAO cromakalin group was administered 10 mg/kg cromakalin(i.p.) prior to MCAO induction.The MCAO+cromakalin+glibenclamide group received an injection of 10 mg/kg cromakalin(i.v.),and subsequently an injection of 10 mg/kg cromakalin(i.p.) prior to MCAO induction.MAIN OUTCOME MEASURES:At 24 hours after cerebral ischemia/reperfusion injury,cellular apoptosis was detected by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate(dUTP) nick-end labeling technique.Cytochrome C expression was measured by immunohistochemistry.In addition,mitochondrial swelling,membrane fluidity,membrane phospholipid and malonaldehyde(MDA) contents,as well as Na^+-K^+-ATPase,Ca^2 +-ATPase,and superoxide dismutase(SOD) activities were determined.RESULTS:Compared with the sham-operated group,the three ischemia groups exhibited significantly elevated mitochondrial MDA content,reduced membrane phospholipid and ATP conten

关 键 词:apoptosis cromakalin cytochrome C energy metabolism MITOCHONDRIA potassium channel/opener 

分 类 号:R741[医药卫生—神经病学与精神病学]

 

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