银杏叶提取物预处理对缺血—再灌注大鼠心肌蛋白质组学的影响
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摘要
第一章银杏叶提取物预处理对大鼠心肌的保护作用
目的：观察银杏叶提取物预处理对缺血再灌注大鼠心肌的保护作用。
方法：健康成年Sprague-Dawley雄性大鼠60只,随机分成3组：S组：假手术组,仅开胸并分离冠状动脉左前降支,但不阻断血流150分钟；IR组：缺血再灌注组,行冠状动脉左前降支阻断30分钟,再灌注120分钟；E组：银杏叶提取物预处理组,予以腹腔注射银杏叶提取物EGB761(100mg/kg),给药后24h同IR组处理。再灌注结束后测心梗面积,观察心肌细胞超微结构变化。
结果：1.心肌梗死面积变化：与IR组(37.87±5.92%)比,E组(24.52±4.13%)心肌梗死面积减小(P<0.05)。2.心肌超微结构变化：与IR组比,E组心肌细胞损伤程度减轻。3.血流动力学变化：与IR组比,E组心功能各项指标提高(P<0.05)。
结论：银杏叶提取物预处理对大鼠缺血再灌注心肌具有保护作用。
第二章银杏叶提取物预处理对缺血再灌注大鼠心肌蛋白质组学的影响
目的：采用蛋白质组学技术探讨银杏叶提取物预处理对大鼠心肌保护的作用机制。
方法：双向凝胶电泳法(2-DE)分离缺血再灌注组(IR组)和银杏叶提取物预处理组(E组)的大鼠心肌蛋白质,对2-DE图谱分析后找出表达差异的蛋白质,并用质谱分析鉴定部分差异蛋白质。结果：经双向凝胶电泳图谱分析发现,IR组的蛋白质点数为894±18,E组的蛋白点数为911±21。其中差异明显的点有14个,经过质谱分析,初步鉴定出11个蛋白质。这些蛋白质包括能量代谢相关蛋白、抗氧化相关蛋白、信号传导相关蛋白及抗凋亡相关蛋白。
结论：银杏叶提取物预处理后心肌组织的蛋白表达发生改变,提示银杏叶提取物预处理的心肌保护作用可能与改善能量代谢、抗氧化反应、抗凋亡等有关。
第三章银杏叶提取物预处理对大鼠心肌囊性纤维化跨膜通道调节因子表达的影响
目的：探讨银杏叶提取物预处理对大鼠心肌缺血再灌注时囊性纤维化跨膜通道调节因子表达的影响。
方法：健康成年Sprague-Dawley雄性大鼠30只,随机分成3组：S组：假手术组,仅开胸并分离冠状动脉左前降支,但不阻断血流150分钟；IR组：缺血再灌注组,行冠状动脉左前降支阻断30分钟,再灌注120分钟；E组：银杏叶提取物预处理组,予以腹腔注射银杏叶提取物(EGB761)100mg/kg,给药后24h同IR组处理。再灌注结束后测心肌囊性纤维化跨膜通道调节因子的表达和心梗面积。
结果：1.心肌梗死面积变化：与IR组(37.87±5.92%)比,E组(24.52±4.13%)心肌梗死面积减小(P<0.05)。2.囊性纤维化跨膜通道调节因子表达变化：与IR组比,E组囊性纤维化跨膜通道调节因子增高(P<0.05)。
结论：银杏叶提取物预处理对大鼠心肌的保护作用可能与上调心肌囊性纤维化跨膜通道调节因子表达有关。
Part one The protection of extract of Ginkgo biloba preconditioning in rat myocardium after ischemic reperfusion.
Objective
To investigate the protection of extract of Ginkgo biloba preconditioning in myocardial ischemia reperfusion injury in the rat.
Methods
Three groups (n=20animals/group) of Sprague-Dawley male rats were studied:group S, control rats that received no treatment; group IR, rats treated with NS (1.0ml/kg ip)24h before ischemia; group E, rats treated with extract of Ginkgo biloba (100mg/kg ip)24h before ischemia. Group IR and E were subjected to ischemia by30min of coronary artery occlusion followed by2h of reperfusion. At the end of the reperfusion, myocardial infarct size was measured. The myocardial ultrastructures were observed under the electron microscopy.
Results
EGB caused a significant reduction in infarct size [24.52+/-4.13vs.37.87+/-5.92%(%area at risk) in controls, P<0.05]. The degree injury of Group E was change better than that of Group IR under the electron microscope.
Conclusion
EGB preconditioning induces the cardioprotection against ischemia reperfusion injury in the rats.
Part two Proteomics analysis of extract of Ginkgo biloba preconditioning in rat myocardium after ischemic reperfusion.
Objective
To investigate the changes of myocardial protein expression after extract of Ginkgo biloba pretreatment, and to search for the mechanism probably involved in the preconditioning of extract of Ginkgo biloba with proteomics techniques.
Methods
Proteomics analysis of myocardium protein of EGB pretreatment. The left ventricle tissues of EGB(group E) or IR(group IR) preconditioned rats were sampled for proteomics analysis. The total proteins were extracted and separated by two dimensional gel elecrtophoresis(2-DE), and differential expression protein spots were analyzed with martix-assisted laser desorption/ionization time-of-flihgt mass spectrometry(MALDI-TOF-MS).
Results
Analysis of2-DE showed that894±18protein spots were in group IR and911±21protein spots in group E, and that the expression of14protein spots were different between the two groups.14protein spots were choosed to do MS analysis, and11proteins were preliminarily identified. These proteins can be classified into four functional groups: metabolism related proteins, anti-oxidant related proteins and others.
Conclusions
EGB preconditioning resulted in the changes of protein expression profiles in the myocardial. The differential proteins might function as anti-oxidant reaction and improve the energy metabolism of myocardial to confer cardioprotection.
Part three Effect of extract of Ginkgo biloba preconditioning on Cystic fibrosis transmembrane conductance regulator expression during myocardial ischemia-reperfusion in rats
Objective
To investigate the effect of extract of Ginkgo biloba preconditioning on Cystic fibrosis transmembrane conductance regulator expression during myocardial ischemia-reperfusion in rats.
Methods
Three groups (n=10animals/group) of Sprague-Dawley male rats were studied:group S, control rats that received no treatment; group IR, rats treated with NS (1.0ml/kg ip)24h before ischemia; group E, rats treated with EGB761(100mg/kg ip)24h before ischemia. Group IR and E were subjected to ischemia by30min of coronary artery occlusion followed by2h of reperfusion. At the end of the reperfusion, myocardial infarct size was measured. Cystic fibrosis transmembrane conductance regulator(CFTR) was measured by Western blotting.
Results
EGB761caused a significant reduction in infarct size [24.52+/-4.13vs.37.87+/-5.92%(%area at risk) in group IR, P<0.05]. EGB761treatment induced the higher expression of CFTR in hearts.
Conclusion
The EGB761preconditioning attenuates myocardial I/R injury possibly through up-regulating CFTR expression in rats.
目的：观察银杏叶提取物预处理对缺血再灌注大鼠心肌的保护作用。
方法：健康成年Sprague-Dawley雄性大鼠60只,随机分成3组：S组：假手术组,仅开胸并分离冠状动脉左前降支,但不阻断血流150分钟；IR组：缺血再灌注组,行冠状动脉左前降支阻断30分钟,再灌注120分钟；E组：银杏叶提取物预处理组,予以腹腔注射银杏叶提取物EGB761(100mg/kg),给药后24h同IR组处理。再灌注结束后测心梗面积,观察心肌细胞超微结构变化。
结果：1.心肌梗死面积变化：与IR组(37.87±5.92%)比,E组(24.52±4.13%)心肌梗死面积减小(P<0.05)。2.心肌超微结构变化：与IR组比,E组心肌细胞损伤程度减轻。3.血流动力学变化：与IR组比,E组心功能各项指标提高(P<0.05)。
结论：银杏叶提取物预处理对大鼠缺血再灌注心肌具有保护作用。
第二章银杏叶提取物预处理对缺血再灌注大鼠心肌蛋白质组学的影响
目的：采用蛋白质组学技术探讨银杏叶提取物预处理对大鼠心肌保护的作用机制。
方法：双向凝胶电泳法(2-DE)分离缺血再灌注组(IR组)和银杏叶提取物预处理组(E组)的大鼠心肌蛋白质,对2-DE图谱分析后找出表达差异的蛋白质,并用质谱分析鉴定部分差异蛋白质。结果：经双向凝胶电泳图谱分析发现,IR组的蛋白质点数为894±18,E组的蛋白点数为911±21。其中差异明显的点有14个,经过质谱分析,初步鉴定出11个蛋白质。这些蛋白质包括能量代谢相关蛋白、抗氧化相关蛋白、信号传导相关蛋白及抗凋亡相关蛋白。
结论：银杏叶提取物预处理后心肌组织的蛋白表达发生改变,提示银杏叶提取物预处理的心肌保护作用可能与改善能量代谢、抗氧化反应、抗凋亡等有关。
第三章银杏叶提取物预处理对大鼠心肌囊性纤维化跨膜通道调节因子表达的影响
目的：探讨银杏叶提取物预处理对大鼠心肌缺血再灌注时囊性纤维化跨膜通道调节因子表达的影响。
方法：健康成年Sprague-Dawley雄性大鼠30只,随机分成3组：S组：假手术组,仅开胸并分离冠状动脉左前降支,但不阻断血流150分钟；IR组：缺血再灌注组,行冠状动脉左前降支阻断30分钟,再灌注120分钟；E组：银杏叶提取物预处理组,予以腹腔注射银杏叶提取物(EGB761)100mg/kg,给药后24h同IR组处理。再灌注结束后测心肌囊性纤维化跨膜通道调节因子的表达和心梗面积。
结果：1.心肌梗死面积变化：与IR组(37.87±5.92%)比,E组(24.52±4.13%)心肌梗死面积减小(P<0.05)。2.囊性纤维化跨膜通道调节因子表达变化：与IR组比,E组囊性纤维化跨膜通道调节因子增高(P<0.05)。
结论：银杏叶提取物预处理对大鼠心肌的保护作用可能与上调心肌囊性纤维化跨膜通道调节因子表达有关。
Part one The protection of extract of Ginkgo biloba preconditioning in rat myocardium after ischemic reperfusion.
Objective
To investigate the protection of extract of Ginkgo biloba preconditioning in myocardial ischemia reperfusion injury in the rat.
Methods
Three groups (n=20animals/group) of Sprague-Dawley male rats were studied:group S, control rats that received no treatment; group IR, rats treated with NS (1.0ml/kg ip)24h before ischemia; group E, rats treated with extract of Ginkgo biloba (100mg/kg ip)24h before ischemia. Group IR and E were subjected to ischemia by30min of coronary artery occlusion followed by2h of reperfusion. At the end of the reperfusion, myocardial infarct size was measured. The myocardial ultrastructures were observed under the electron microscopy.
Results
EGB caused a significant reduction in infarct size [24.52+/-4.13vs.37.87+/-5.92%(%area at risk) in controls, P<0.05]. The degree injury of Group E was change better than that of Group IR under the electron microscope.
Conclusion
EGB preconditioning induces the cardioprotection against ischemia reperfusion injury in the rats.
Part two Proteomics analysis of extract of Ginkgo biloba preconditioning in rat myocardium after ischemic reperfusion.
Objective
To investigate the changes of myocardial protein expression after extract of Ginkgo biloba pretreatment, and to search for the mechanism probably involved in the preconditioning of extract of Ginkgo biloba with proteomics techniques.
Methods
Proteomics analysis of myocardium protein of EGB pretreatment. The left ventricle tissues of EGB(group E) or IR(group IR) preconditioned rats were sampled for proteomics analysis. The total proteins were extracted and separated by two dimensional gel elecrtophoresis(2-DE), and differential expression protein spots were analyzed with martix-assisted laser desorption/ionization time-of-flihgt mass spectrometry(MALDI-TOF-MS).
Results
Analysis of2-DE showed that894±18protein spots were in group IR and911±21protein spots in group E, and that the expression of14protein spots were different between the two groups.14protein spots were choosed to do MS analysis, and11proteins were preliminarily identified. These proteins can be classified into four functional groups: metabolism related proteins, anti-oxidant related proteins and others.
Conclusions
EGB preconditioning resulted in the changes of protein expression profiles in the myocardial. The differential proteins might function as anti-oxidant reaction and improve the energy metabolism of myocardial to confer cardioprotection.
Part three Effect of extract of Ginkgo biloba preconditioning on Cystic fibrosis transmembrane conductance regulator expression during myocardial ischemia-reperfusion in rats
Objective
To investigate the effect of extract of Ginkgo biloba preconditioning on Cystic fibrosis transmembrane conductance regulator expression during myocardial ischemia-reperfusion in rats.
Methods
Three groups (n=10animals/group) of Sprague-Dawley male rats were studied:group S, control rats that received no treatment; group IR, rats treated with NS (1.0ml/kg ip)24h before ischemia; group E, rats treated with EGB761(100mg/kg ip)24h before ischemia. Group IR and E were subjected to ischemia by30min of coronary artery occlusion followed by2h of reperfusion. At the end of the reperfusion, myocardial infarct size was measured. Cystic fibrosis transmembrane conductance regulator(CFTR) was measured by Western blotting.
Results
EGB761caused a significant reduction in infarct size [24.52+/-4.13vs.37.87+/-5.92%(%area at risk) in group IR, P<0.05]. EGB761treatment induced the higher expression of CFTR in hearts.
Conclusion
The EGB761preconditioning attenuates myocardial I/R injury possibly through up-regulating CFTR expression in rats.
引文
[1]Murry CE, Jennings RB, Reimer KA.Preconditioning with ischemia:a delay of lehtal cell injuy in ischemic myocardium.Cicrulation,1986,74 (5):1124-1136.
[2]GrossER, HsuAK, GrossGJ. The JAK/STAT pathway is essential for opioid-induced cardioprotection:JAK2 as a mediator of STAT3, Akt, and GSK-3 beta. Am J Physiol Heart Circ Physiol,2006,291(2):H827-34.
[3]Tosaka S, Tosaka R, Matsumoto S, et al. Roles of cyclooxygenase 2 in sevoflurane-and olprinone-induced early phase of preconditioning and postconditioning against myocardial infarction in rat hearts. Cardiovasc Pharmacol Ther,2011,16(1):72-8.
[4]Liao X, Wang L, Yang C, et al. Cyclooxygenase mediates cardioprotection of angiotensin-(1-7) against ischemia/reperfusion-induced injury through the inhibition of oxidative stress.Mol Med Report,2011,4(6):1145-50.
[5]Wang X, Fisher PW, Xi L, et al. Essential role of mitochondrial Ca2+-activated and ATP-sensitive K+ channels in sildenafil-induced late cardioprotection.J Mol Cell Cardiol,,44(1):105-13.
[6]Hennan JK, Driscoll EM, Barrett TD, et al. Effect of sodium/hydrogen exchange inhibition on myocardial infarct size after coronary artery thrombosis and thrombolysis.Pharmacology,2006,78(1):27-37.
[7]Bolli R. The late Phase of Perconditioning.Cicr Res,2000,87(11):972-983.
[8]Rizvi A, Tang XL, Qiu Y, et al.Increased Protein synthesis is necessary forthe development of late preconditioning against myocardial stunning[J].Am J Phy siol,1999,277(32):874-884.
[9]Wilkins MR, Sanchez JC, Gooley AA, et al. Progress with proteome projects:why all proteins expressed by a genome should be identified and how to do it. J Biotechnol Genet Eng Rev,1996,13:19-50.
[10]Arrenll DK, Neverova I, Van Eyk JE.Cardiovascular Proteomic:evolution and potential.Circ Res,2001,88(8):763-773.
[11]De Feudis FV.Ginkgo biloba extract(EGb761):pharmacological cativaties and clinical applications[J].Elsevier,1991.
[12]De Feudis FV.Fromchemistryto clinic.Wiesbaden,Germany Ullstoin edical,1998; 7:11.
[13]Li CL,Wong YY.The bioavailability of ginkgolides and Ginkgo biloba extracts[J]. Planta Med,1997;63:563-565.
[14]Guillon JM,Rochette L,Baranes H.Effects of Ginkgo biloba extract on two models of experimental myocardial ischemia[J]. Presse Med,1986;15(31):1516.
[15]Tosaki A,Engel man DT,Pali T,et al.Ginkgo biloba extract (EGB761) improves posrischenic function in isolated preconditioned working rat heart[J].Coron Artery Dis;1994,5(5):443.
[16]潘晓岩.银杏叶提取物对离体大鼠心脏再灌注心律失常的影响[J].中国药理学通报,1998,14(3)：283-285.
[17]Baxter GF, Goma FM, Yellon DM. Characterisation of the infarct-limiting effect of delayed preconditioning:timecourse and dose-dependency studies in rabbit myocardium. Basic Res Cardiol,1997,92(3):159-67.
[18]Tang XL, Qiu Y, Park SW, et al. Time course of late preconditioning against myocardial stunning in conscious pigs. Circ Res,1996,79:424-434.
[19]殷仁富,陈金明,主编.心脏能量学：代谢与治疗.第1版.上海：第二军医大学出版社,2002.103,J13.
[20]Shen J, Wang J, Zhao B, et al. Effects of EGb 761 on nitric oxide and oxygen free radicals, myocardial damage and arrhythmia in ischemia-reperfusion injury in vivo. Biochim Biophys Acta,1998,1406(3):228-36.
[21]Rioufol G, Pietri S, Culcasi M, et al.Ginkgo biloba extract EGb 761 attenuates myocardial stunning in the pig heart. Basic Res Cardiol,2003,98(1):59-68.
[22]Varga E, Bodi A, Ferdinandy P, et al. The protective effect of EGb 761 in isolated ischemic/reperfused rat hearts:a link between cardiac function and nitric oxide production. J Cardiovasc Pharmacol,1999,34(5):711-7.
[23]Ohtake M,Morino S,Kaidoh T,et al.Three-dimensional structural changes in cerebral microvessels after transient focal cerebral ischemia in rats:scanning electron microscopic study of corrosion casts.Neuropa theology,2004,24(3):219-227.
[24]Zaugg M, Lucchinetti E, Garcia C, et al. Anaesthetics and cardiac preconditioning. Clinical implications,Br J Anaesth,2003,91:566-76.
[25]Rao PS, Cohen MV, Mueller HS, et al.Production of free radicals and lipid peroxides in early experimental myocardial ischemia. J Mol Cell Cardiol,1983,15: 713.
[26]Przylenk K, Li G, Whittaker P. No loss in the in vivo efficacy of ischemic preconditioning in middle-aged and old rabbits.J Am Coll Cardiol, 2001,38(6):1741-1747.
[27]Cohen MV. Efficacy of preconditioning should be gauged by reduction of infarction. Br J Pharmacol,2004,141(2):197-198.
[1]Bannai H, Fukatsu K, Mizutani A. An RNA-interacting protein, SYNCRIP (heterogeneous nuclear ribonulear protein Q1/NSAP1)is a component of mRNA granule transported with inositol 1,4,5-trisphosphate receptor type 1 mRNA in neuronal dendrites. J Biol Chem,2004,17,279(51):53427-53434.
[2]Vercauteren FG, Clerens S, Roy L. Early dysregulation of hippocampal protein in transgenic rats with Alzheimer disease-linked mutations in amyloid precursor protein and presenilin 1.Brain Res Mol,2004 Dec 20,132(2):241-59.
[3]Gorg A, Obermaier C, Boguth G, et al. The current state of two-dimensional electrophoresis with immobilized PH gradients. Electrophoresis.2000,21:1037-1053.
[4]Decca MB, Bosc C, Luche S. Protein arginylation in rat brain cytosol:a proteomic analysis. Neurochem Res.2006 Mar;31(3):401-9.
[5]Hwang YY, Li MD.Proteins differentially expressed in response to nicotine in five rat brain regions:identification using a 2-DE/MS-based proteomics approach. proteomics.2006 May,6(10):31318-53.
[6]Reifschneider NH, Goto S, Nakamoto H. Defining the mitochondrial proteomes from five rat organs in a physiologically significant context using 2D blue-native/SDS-PAGE. J Proteome Res.2006 May,5(5):1117-32.
[7]Arrell DK, Elliott ST, Kane LA, et al. Proteomic analysis of pharmacological precondioning:novel protein targets converge to mitoehondrial metabolism pathways. Circ Res,2006,99(7):706-714.
[8]Guillon JM,Rochette L,Baranes H.Effects of Ginkgo biloba extract on two models of experimental myocardial ischemia. Presse Med,1986,15(31):1516.
[9]Tosaki A,Engel man DT,Pali T,et al.Ginkgo biloba extract (EGB761) improves posrischenic function in isolated preconditioned working rat heart. Coron Artery Dis,1994,5(5):443.
[10]潘晓岩.银杏叶提取物对离体大鼠心脏再灌注心律失常的影响.中国药理学通报,1998,14(3)：283-285.
[11]Sam Hanash. Disease proteomics. Nature,2003,422:226-232.
[12]Wulfkuhle JD, Paweletz CP, Steeg PS, et al. Proteomic approaches to the diagnosis, treatment, and monitoring of Cancer. Adv Exp Med Biol,2003,532:59-68.
[13]Page M, Amess B, Rohlff C, et al. Proteomics:a major new technology for the drug discovery process. Drug Discov Today,1999,4:55-62.
[14]Wang JH, Hewick RM. Proteomics in drug discovery. Drug Discov Today,1999,4:129-133.
[15]Molloy MP. Two dimensional electrophoresis of membrane proteins using immobilized pH gradients. Anal Biochem,2000,280:
[16]Klein E, Klein JB, Thongboonkerd V,et al. Two dimensionalgel electrophoresis:a fundamental tool for expression protemics studies.Conirib Nephrol,2004,141:25.
[17]Lim MS, Elenitoba-Johnson KS.Proteomics in pathology research.Lab Invest,2004,141:25.
[18]Tyers M, Mann M. From genomics to proteomics. Nature,2003,422 (6928): 193-197.
[19]Randall MD, Keon CA, Greenhaff PL et al. Dual effects of dichloroacetate on cardiac ischaemic preconditioning in the rat isolated perfused heart. Br J Pharmacol 1998;124(1):245-51.
[20]Saiki Y, Lopaschuk GD, Dodge K et al. Pyruvate augments mechanical function via activation of the pyruvate dehydrogenase complex in reperfused ischemic immature rabbit hearts. J Surg Res 1998;79(2):164-9.
[21]张振英,刘秀华,孙胜,等.腹主动脉狭窄致大鼠心肌肥大后心肌组织蛋白质组变化的研究.中国微循环,2009,13(2)：84-89.
[22]Fert-Bober J, Sawicki G, Lopaschuk GD et al. Proteomic analysis of cardiac metabolic enzymes in asphyxiated newborn piglets. Mol Cell Biochem,2008,318 (1-2):13-21.
[23]Popova T, Pinheiro de Carvalho MA, Matasova L et al. Regulation of mitochondrial NADP-isocitrate dehydrogenase in rat heart during ischemia. Mol Cell Biochem,2007,294(1-2):97-105.
[24]Ito H, Nakano A, Kinoshita M,et al. Pioglitazone,a peroxisome proliferator-activated receptor-gamma agonist,attenuates myocardial ischemia reperfusion injury in a rat model. Lab Invest,2003,83(12):17-15.
[25]Liu HR, Tao L, Gao E,et al. Anti-apoptotic effects of rosiglitazone in hypercholesterolemic rabbits subjected to myocardial ischemia and reperfusion. Cardiovasc Res,2004,62(1):135.
[26]Yue TL, Chen J, Bao W, et al. In vivo myocardial protection from ischemia reperfusion injury by the peroxisome prolife rat or-activated receptor-gamma agonist rosiglitazone.Circulation,2001,104(21):2588.
[27]Naito Y, Yoshikawa T. Thiazolidinediones:a new class of drugs for the therapy of ischemia-reperfusion injury. Drugs Today(Barc),2004,40(5):423.
[28]Duan DY, Liu LL, Bozeat N,et al. Functional role of anion channels in cardiac diseases. Acta Pharmacol Sin.2005 Mar;26(3):265-78.
[29]Chen H, Liu LL, Ye LL, Targeted inactivation of cystic fibrosis transmembrane conductance regulator chloride channel gene prevents ischemic preconditioning in isolated mouse heart. Circulation,2004,10,110(6):700-4
[30]Xiang SY, Ye LL, Duan LL, et al. Characterization of a critical role for CFTR chloride channels in cardioprotection against ischemia/reperfusion injury. Acta Pharmacol Sin,2011,32(6):824-33.
[31]Hume JR, Duan D, Collier ML, et al. Anion transport in heart. Physiol Rev.2000; 80:31-81.
[32]Ruiz PE, Ponce ZA, Schanne OF. Early action potential shortening in hypoxic hearts:role of chloride current(s) mediated by catecholamine release. J Mol Cell Cardiol.1996; 28:279-290.
[33]Barriere H, Poujeol C, Tauc M, et al. CFTR modulates programmed cell death by decreasing intracellular pH in Chinese hamster lung fibroblasts. Am J Physiol. 2001; 281:C810-C824.
[34]Valverde MA, Vazquez E, Munoz FJ, et al. Murine CFTR channel and its role in regulatory volume decrease of small intestine crypts. Cell Physiol Biochem.2000; 10:321-328.
[35]Jacquelyne A, Kazuo A, Morgan AR.Fluorometric assays for DNAtopoisomerases and topoisomerase-targeted drugs:quantitation of catalytic activity and DNA cleavage. Molecular Pharmacology,1991,40:495.
[36]Xiaojian W, Nan L, Bin L, et al.A novel Human PhosPhatidylethanolamine-binding protein resists Tumor Necrosis Factor-indueed apotosis by inhibiting mitogen-activated protein kinase pathway activation and phosphatidylethanolamine externalization.J Biol Chem,2004,279:45855-45864.
[37]Li P, Wang X, Li N, et al. Anti-apoptotic hPEBP4 silencing promotes TRAIL-induced apoptosis of human ovarian cancer cells by activating ERK and JNK pathways. Int J Mol Med,2006,18(3):505-510.
[1]Duan DY, Liu LL, Bozeat N,et al. Functional role of anion channels in cardiac diseases. Acta Pharmacol Sin.2005 Mar;26(3):265-78.
[2]Chen H, Liu LL, Ye LL, Targeted inactivation of cystic fibrosis transmembrane conductance regulator chloride channel gene prevents ischemic preconditioning in isolated mouse heart. Circulation,2004,10,110(6):700-4
[3]Xiang SY, Ye LL, Duan LL, et al. Characterization of a critical role for CFTR chloride channels in cardioprotection against ischemia/reperfusion injury. Acta Pharmacol Sin,2011,32(6):824-33.
[4]Hume JR, Duan D, Collier ML, et al. Anion transport in heart. Physiol Rev.2000; 80:31-81.
[5]Ruiz PE, Ponce ZA, Schanne OF. Early action potential shortening in hypoxic hearts:role of chloride current(s) mediated by catecholamine release. J Mol Cell Cardiol.1996; 28:279-290.
[6]Barriere H, Poujeol C, Tauc M, et al. CFTR modulates programmed cell death by decreasing intracellular pH in Chinese hamster lung fibroblasts. Am J Physiol. 2001; 281:C810-C824.
[7]Valverde MA, Vazquez E, Munoz FJ, et al. Murine CFTR channel and its role in regulatory volume decrease of small intestine crypts. Cell Physiol Biochem.2000; 10:321-328.
[1]. Jennings RB, Reimer KA. Factors involved in salvaging ischemic myocardium: effect of reperfusion of arterial blood[J]. Circulation,1983,68(2 Pt 2):Ⅰ25-36.
[2]. Braunwald E, Kloner RA. Myocardial reperfusion:a double-edged sword?[J]. J Clin Invest,1985,76(5):1713-9.
[3]. Kloner RA. Does reperfusion injury exist in humans?[J]. J Am Coll Cardiol, 1993,21(2):537-45.
[4]. Schafer C, Ladilov Y, Inserte J et al. Role of the reverse mode of the Na+/Ca2+ exchanger in reoxygenation-induced cardiomyocyte injury[J]. Cardiovasc Res, 2001,51(2):241-50.
[5]. Gumina RJ, Buerger E, Eickmeier C et al. Inhibition of the Na(+)/H(+) exchanger confers greater cardioprotection against 90 minutes of myocardial ischemia than ischemic preconditioning in dogs[J]. Circulation,1999,100(25):2519-26; discussion 469-72.
[6]. Zeymer U, Suryapranata H, Monassier JP et al. The Na(+)/H(+) exchange inhibitor eniporide as an adjunct to early reperfusion therapy for acute myocardial infarction. Results of the evaluation of the safety and cardioprotective effects of eniporide in acute myocardial infarction (ESCAMI) trial[J]. J Am Coll Cardiol, 2001,38(6):1644-50.
[7]. Garcia-Dorado D, Inserte J, Ruiz-Meana M et al. Gap junction uncoupler heptanol prevents cell-to-cell progression of hypercontracture and limits necrosis during myocardial reperfusion[J]. Circulation,1997,96(10):3579-86.
[8]. Schulz R, Gres P, Skyschally A et al. Ischemic preconditioning preserves connexin 43 phosphorylation during sustained ischemia in pig hearts in vivo[J]. FASEB J,2003,17(10):1355-7.
[9]. Zweier JL, Talukder MA. The role of oxidants and free radicals in reperfusion injury[J]. Cardiovasc Res,2006,70(2):181-90.
[10]. Akizuki S, Yoshida S, Chambers DE et al. Infarct size limitation by the xanthine oxidase inhibitor, allopurinol, in closed-chest dogs with small infarcts[J]. Cardiovasc Res,1985,19(11):686-92.
[11]. Uraizee A, Reimer KA, Murry CE et al. Failure of superoxide dismutase to limit size of myocardial infarction after 40 minutes of ischemia and 4 days of reperfusion in dogs[J]. Circulation,1987,75(6):1237-48.
[12]. Ishii H, Ichimiya S, Kanashiro M et al. Impact of a single intravenous administration of nicorandil before reperfusion in patients with ST-segment-elevation myocardial infarction[J]. Circulation,2005,112(9):1284-8.
[13]. Kitakaze M, Asakura M, Kim J et al. Human atrial natriuretic peptide and nicorandil as adjuncts to reperfusion treatment for acute myocardial infarction (J-WIND):two randomised trials[J]. Lancet,2007,370(9597):1483-93.
[14]. Liang F, Gao E, Tao L et al. Critical timing of L-arginine treatment in post-ischemic myocardial apoptosis-role of NOS isoforms[J]. Cardiovasc Res, 2004,62(3):568-77.
[15]. Garcia-Dorado D, Rodriguez-Sinovas A, Ruiz-Meana M et al. The end-effectors of preconditioning protection against myocardial cell death secondary to ischemia-reperfusion[J]. Cardiovasc Res,2006,70(2):274-85.
[16]. Bond JM, Herman B, Lemasters JJ. Protection by acidotic pH against anoxia/reoxygenation injury to rat neonatal cardiac myocytes[J]. Biochem Biophys Res Commun,1991,179(2):798-803.
[17]. Petzelbauer P, Zacharowski PA, Miyazaki Y et al. The fibrin-derived peptide Bbetal5-42 protects the myocardium against ischemia-reperfusion injury[J]. Nat Med,2005,11(3):298-304.
[18]. Armstrong PW, Granger CB, Adams PX et al. Pexelizumab for acute ST-elevation myocardial infarction in patients undergoing primary percutaneous coronary intervention:a randomized controlled trial[J]. JAMA,2007,297(1): 43-51.
[19]. Griffiths EJ, Halestrap AP. Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion[J]. Biochem J,1995,307 (Pt 1)(93-8.
[20]. Spisani S, Fabbri E, Muccinelli M et al. Inhibition of neutrophil responses by cyclosporin A. An insight into molecular mechanisms[J]. Rheumatology (Oxford), 2001,40(7):794-800.
[21]. Piot C, Croisille P, Staat P et al. Effect of cyclosporine on reperfusion injury in acute myocardial infarction[J]. N Engl J Med,2008,359(5):473-81.
[22]. Hausenloy DJ, Yellon DM. Reperfusion injury salvage kinase signalling:taking a RISK for cardioprotection[J]. Heart Fail Rev,2007,12(3-4):217-34.
[23]. Heusch G, Boengler K, Schulz R. Cardioprotection:nitric oxide, protein kinases, and mitochondria[J]. Circulation,2008,118(19):1915-9.
[24]. Daemen MA, van't Veer C, Denecker G et al. Inhibition of apoptosis induced by ischemia-reperfusion prevents inflammation[J]. J Clin Invest,1999,104(5):541-9.
[25]. Matsui Y, Takagi H, Qu X et al. Distinct roles of autophagy in the heart during ischemia and reperfusion:roles of AMP-activated protein kinase and Beclin 1 in mediating autophagy[J]. Circ Res,2007,100(6):914-22.
[26]. Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia:a delay of lethal cell injury in ischemic myocardium[J]. Circulation,1986,74(5):1124-36.
[27]. Kuzuya T, Hoshida S, Yamashita N et al. Delayed effects of sublethal ischemia on the acquisition of tolerance to ischemia[J]. Circ Res,1993,72(6):1293-9.
[28]. Liu GS, Thornton J, Van Winkle DM et al. Protection against infarction afforded by preconditioning is mediated by A1 adenosine receptors in rabbit heart[J]. Circulation,1991,84(1):350-6.
[29]. Ganote CE, Armstrong S, Downey JM. Adenosine and A1 selective agonists offer minimal protection against ischaemic injury to isolated rat cardiomyocytes[J]. Cardiovasc Res,1993,27(9):1670-6.
[30]. Yitzhaki S, Huang C, Liu W et al. Autophagy is required for preconditioning by the adenosine A1 receptor-selective agonist CCPA[J]. Basic Res Cardiol, 2009,104(2):157-67.
[31]. Hori M, Kitakaze M, Sato H et al. Staged reperfusion attenuates myocardial stunning in dogs. Role of transient acidosis during early reperfusion[J]. Circulation,1991,84(5):2135-45.
[32].Tong H, Bernstein D, Murphy E et al. The role of beta-adrenergic receptor signaling in cardioprotection[J]. FASEB J,2005,19(8):983-5.
[33]. Thornton JD, Daly JF, Cohen MV et al. Catecholamines can induce adenosine receptor-mediated protection of the myocardium but do not participate in ischemic preconditioning in the rabbit[J]. Circ Res,1993,73(4):649-55.
[34]. Kudej RK, Shen YT, Peppas AP et al. Obligatory role of cardiac nerves and alpha 1-adrenergic receptors for the second window of ischemic preconditioning in conscious pigs[J]. Circ Res,2006,99(11):1270-6.
[35]. Sanada S, Komuro I, Kitakaze M. Pathophysiology of myocardial reperfusion injury:preconditioning, postconditioning, and translational aspects of protective measures[J]. Am J Physiol Heart Circ Physiol,301(5):H1723-41.
[36]. Ytrehus K, Liu Y, Downey JM. Preconditioning protects ischemic rabbit heart by protein kinase C activation[J]. Am J Physiol,1994,266(3 Pt 2):H1145-52.
[37]. Sanada S, Asanuma H, Tsukamoto O et al. Protein kinase A as another mediator of ischemic preconditioning independent of protein kinase C[J]. Circulation, 2004,110(1):51-7.
[38]. Sivaraman V, Hausenloy DJ, Kolvekar S et al. The divergent roles of protein kinase C epsilon and delta in simulated ischaemia-reperfusion injury in human myocardium[J]. J Mol Cell Cardiol,2009,46(5):758-64.
[39]. Kitakaze M, Hori M. It is time to ask what adenosine can do for cardioprotection[J]. Heart Vessels,1998,13(5):211-28.
[40]. Saxena M, Williams S, Tasken K et al. Crosstalk between cAMP-dependent kinase and MAP kinase through a protein tyrosine phosphatase[J]. Nat Cell Biol, 1999,1(5):305-11.
[41]. Sanada S, Kitakaze M, Papst PJ et al. Cardioprotective effect afforded by transient exposure to phosphodiesterase Ⅲ inhibitors:the role of protein kinase A and p38 mitogen-activated protein kinase[J]. Circulation,2001,104(6):705-10.
[42]. Saurin AT, Martin JL, Heads RJ et al. The role of differential activation of p38-mitogen-activated protein kinase in preconditioned ventricular myocytes[J]. FASEB J,2000,14(14):2237-46.
[43]. Behrends M, Schulz R, Post H et al. Inconsistent relation of MAPK activation to infarct size reduction by ischemic preconditioning in pigs[J]. Am J Physiol Heart Circ Physiol,2000,279(3):H1111-9.
[44]. Boengler K, Buechert A, Heinen Y et al. Cardioprotection by ischemic postconditioning is lost in aged and STAT3-deficient mice[J]. Circ Res, 2008,102(1):131-5.
[45]. Cohen MV, Yang XM, Liu Y et al. Cardioprotective PKG-independent NO signaling at reperfusion[J]. Am J Physiol Heart Circ Physiol, 2010,299(6):H2028-36.
[46]. Sanada S, Node K, Asanuma H et al. Opening of the adenosine triphosphate-sensitive potassium channel attenuates cardiac remodeling induced by long-term inhibition of nitric oxide synthesis:role of 70-kDa S6 kinase and extracellular signal-regulated kinase[J]. J Am Coll Cardiol,2002,40(5):991-7.
[47]. Costa AD, Garlid KD. Intramitochondrial signaling:interactions among mitoKATP, PKCepsilon, ROS, and MPT[J]. Am J Physiol Heart Circ Physiol, 2008,295(2):H874-82.
[48]. Halestrap AP, Pasdois P. The role of the mitochondrial permeability transition pore in heart disease[J]. Biochim Biophys Acta,2009,1787(11):1402-15.
[49]. Halestrap AP. What is the mitochondrial permeability transition pore?[J]. J Mol Cell Cardiol,2009,46(6):821-31.
[50]. Ovize M, Baxter GF, Di Lisa F et al. Postconditioning and protection from reperfusion injury:where do we stand? Position paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology[J]. Cardiovasc Res,2010,87(3):406-23.
[51]. Manintveld OC, Te Lintel Hekkert M, van den Bos EJ et al. Cardiac effects of postconditioning depend critically on the duration of index ischemia[J]. Am J Physiol Heart Circ Physiol,2007,292(3):H1551-60.
[52]. Kharbanda RK, Mortensen UM, White PA et al. Transient limb ischemia induces remote ischemic preconditioning in vivo[J]. Circulation,2002,106(23):2881-3.
[53]. Przyklenk K, Bauer B, Ovize M et al. Regional ischemic 'preconditioning' protects remote virgin myocardium from subsequent sustained coronary occlusion[J]. Circulation,1993,87(3):893-9.
[54]. Birnbaum Y, Hale SL, Kloner RA. Ischemic preconditioning at a distance: reduction of myocardial infarct size by partial reduction of blood supply combined with rapid stimulation of the gastrocnemius muscle in the rabbit[J]. Circulation, 1997,96(5):1641-6.
[55]. Bartel DP. MicroRNAs:target recognition and regulatory functions[J]. Cell, 2009,136(2):215-33.
[56]. Eulalio A, Huntzinger E, Izaurralde E. Getting to the root of miRNA-mediated gene silencing[J]. Cell,2008,132(1):9-14.
[57]. Zhao Y, Ransom JF, Li A et al. Dysregulation of cardiogenesis, cardiac conduction, and cell cycle in mice lacking miRNA-1-2[J]. Cell, 2007,129(2):303-17.
[58]. Thum T, Galuppo P, Wolf C et al. MicroRNAs in the human heart:a clue to fetal gene reprogramming in heart failure[J]. Circulation,2007,116(3):258-67.
[59].Cordes KR, Srivastava D. MicroRNA regulation of cardiovascular development[J]. Circ Res,2009,104(6):724-32.
[60]. Fichtlscherer S, De Rosa S, Fox H et al. Circulating microRNAs in patients with coronary artery disease[J]. Circ Res,2010,107(5):677-84.
[61]. Tang Y, Zheng J, Sun Y et al. MicroRNA-1 regulates cardiomyocyte apoptosis by targeting Bcl-2[J]. Int Heart J,2009,50(3):377-87.
[62]. Xu C, Lu Y, Pan Z et al. The muscle-specific microRNAs miR-1 and miR-133 produce opposing effects on apoptosis by targeting HSP60, HSP70 and caspase-9 in cardiomyocytes[J]. J Cell Sci,2007,120(Pt 17):3045-52.
[63]. Wang Y, Lee CG. MicroRNA and cancer--focus on apoptosis[J]. J Cell Mol Med, 2009,13(1):12-23.
[64]. Ren XP, Wu J, Wang X et al. MicroRNA-320 is involved in the regulation of cardiac ischemia/reperfusion injury by targeting heat-shock protein 20[J]. Circulation,2009,119(17):2357-66.
[65]. Bonauer A, Carmona G, Iwasaki M et al. MicroRNA-92a controls angiogenesis and functional recovery of ischemic tissues in mice[J]. Science, 2009,324(5935):1710-3.
[66]. Wang S, Aurora AB, Johnson BA et al. The endothelial-specific microRNA miR-126 governs vascular integrity and angiogenesis[J]. Dev Cell, 2008,15(2):261-71.
[67]. Yin C, Salloum FN, Kukreja RC. A novel role of microRNA in late preconditioning:upregulation of endothelial nitric oxide synthase and heat shock protein 70[J]. Circ Res,2009,104(5):572-5.
[68]. Dong S, Cheng Y, Yang J et al. MicroRNA expression signature and the role of microRNA-21 in the early phase of acute myocardial infarction[J]. J Biol Chem, 2009,284(43):29514-25.
[69]. Sayed D, He M, Hong C et al. MicroRNA-21 is a downstream effector of AKT that mediates its antiapoptotic effects via suppression of Fas ligand[J]. J Biol Chem,2010,285(26):20281-90.
[70]. He L, Lemasters JJ. Heat shock suppresses the permeability transition in rat liver mitochondria[J]. J Biol Chem,2003,278(19):16755-60.
[71]. Ivan M, Haberberger T, Gervasi DC et al. Biochemical purification and pharmacological inhibition of a mammalian prolyl hydroxylase acting on hypoxia-inducible factor[J]. Proc Natl Acad Sci U S A,2002,99(21):13459-64.
[72]. Ockaili R, Natarajan R, Salloum F et al. HIF-1 activation attenuates postischemic myocardial injury:role for heme oxygenase-1 in modulating micro vascular chemokine generation[J]. Am J Physiol Heart Circ Physiol, 2005,289(2):H542-8.
[73]. Natarajan R, Salloum FN, Fisher BJ et al. Hypoxia inducible factor-1 activation by prolyl 4-hydroxylase-2 gene silencing attenuates myocardial ischemia reperfusion injury[J]. Circ Res,2006,98(1):133-40.
[74]. Rane S, He M, Sayed D et al. Downregulation of miR-199a derepresses hypoxia-inducible factor-1 alpha and Sirtuin 1 and recapitulates hypoxia preconditioning in cardiac myocytes[J]. Circ Res,2009,104(7):879-86.
[2]GrossER, HsuAK, GrossGJ. The JAK/STAT pathway is essential for opioid-induced cardioprotection:JAK2 as a mediator of STAT3, Akt, and GSK-3 beta. Am J Physiol Heart Circ Physiol,2006,291(2):H827-34.
[3]Tosaka S, Tosaka R, Matsumoto S, et al. Roles of cyclooxygenase 2 in sevoflurane-and olprinone-induced early phase of preconditioning and postconditioning against myocardial infarction in rat hearts. Cardiovasc Pharmacol Ther,2011,16(1):72-8.
[4]Liao X, Wang L, Yang C, et al. Cyclooxygenase mediates cardioprotection of angiotensin-(1-7) against ischemia/reperfusion-induced injury through the inhibition of oxidative stress.Mol Med Report,2011,4(6):1145-50.
[5]Wang X, Fisher PW, Xi L, et al. Essential role of mitochondrial Ca2+-activated and ATP-sensitive K+ channels in sildenafil-induced late cardioprotection.J Mol Cell Cardiol,,44(1):105-13.
[6]Hennan JK, Driscoll EM, Barrett TD, et al. Effect of sodium/hydrogen exchange inhibition on myocardial infarct size after coronary artery thrombosis and thrombolysis.Pharmacology,2006,78(1):27-37.
[7]Bolli R. The late Phase of Perconditioning.Cicr Res,2000,87(11):972-983.
[8]Rizvi A, Tang XL, Qiu Y, et al.Increased Protein synthesis is necessary forthe development of late preconditioning against myocardial stunning[J].Am J Phy siol,1999,277(32):874-884.
[9]Wilkins MR, Sanchez JC, Gooley AA, et al. Progress with proteome projects:why all proteins expressed by a genome should be identified and how to do it. J Biotechnol Genet Eng Rev,1996,13:19-50.
[10]Arrenll DK, Neverova I, Van Eyk JE.Cardiovascular Proteomic:evolution and potential.Circ Res,2001,88(8):763-773.
[11]De Feudis FV.Ginkgo biloba extract(EGb761):pharmacological cativaties and clinical applications[J].Elsevier,1991.
[12]De Feudis FV.Fromchemistryto clinic.Wiesbaden,Germany Ullstoin edical,1998; 7:11.
[13]Li CL,Wong YY.The bioavailability of ginkgolides and Ginkgo biloba extracts[J]. Planta Med,1997;63:563-565.
[14]Guillon JM,Rochette L,Baranes H.Effects of Ginkgo biloba extract on two models of experimental myocardial ischemia[J]. Presse Med,1986;15(31):1516.
[15]Tosaki A,Engel man DT,Pali T,et al.Ginkgo biloba extract (EGB761) improves posrischenic function in isolated preconditioned working rat heart[J].Coron Artery Dis;1994,5(5):443.
[16]潘晓岩.银杏叶提取物对离体大鼠心脏再灌注心律失常的影响[J].中国药理学通报,1998,14(3)：283-285.
[17]Baxter GF, Goma FM, Yellon DM. Characterisation of the infarct-limiting effect of delayed preconditioning:timecourse and dose-dependency studies in rabbit myocardium. Basic Res Cardiol,1997,92(3):159-67.
[18]Tang XL, Qiu Y, Park SW, et al. Time course of late preconditioning against myocardial stunning in conscious pigs. Circ Res,1996,79:424-434.
[19]殷仁富,陈金明,主编.心脏能量学：代谢与治疗.第1版.上海：第二军医大学出版社,2002.103,J13.
[20]Shen J, Wang J, Zhao B, et al. Effects of EGb 761 on nitric oxide and oxygen free radicals, myocardial damage and arrhythmia in ischemia-reperfusion injury in vivo. Biochim Biophys Acta,1998,1406(3):228-36.
[21]Rioufol G, Pietri S, Culcasi M, et al.Ginkgo biloba extract EGb 761 attenuates myocardial stunning in the pig heart. Basic Res Cardiol,2003,98(1):59-68.
[22]Varga E, Bodi A, Ferdinandy P, et al. The protective effect of EGb 761 in isolated ischemic/reperfused rat hearts:a link between cardiac function and nitric oxide production. J Cardiovasc Pharmacol,1999,34(5):711-7.
[23]Ohtake M,Morino S,Kaidoh T,et al.Three-dimensional structural changes in cerebral microvessels after transient focal cerebral ischemia in rats:scanning electron microscopic study of corrosion casts.Neuropa theology,2004,24(3):219-227.
[24]Zaugg M, Lucchinetti E, Garcia C, et al. Anaesthetics and cardiac preconditioning. Clinical implications,Br J Anaesth,2003,91:566-76.
[25]Rao PS, Cohen MV, Mueller HS, et al.Production of free radicals and lipid peroxides in early experimental myocardial ischemia. J Mol Cell Cardiol,1983,15: 713.
[26]Przylenk K, Li G, Whittaker P. No loss in the in vivo efficacy of ischemic preconditioning in middle-aged and old rabbits.J Am Coll Cardiol, 2001,38(6):1741-1747.
[27]Cohen MV. Efficacy of preconditioning should be gauged by reduction of infarction. Br J Pharmacol,2004,141(2):197-198.
[1]Bannai H, Fukatsu K, Mizutani A. An RNA-interacting protein, SYNCRIP (heterogeneous nuclear ribonulear protein Q1/NSAP1)is a component of mRNA granule transported with inositol 1,4,5-trisphosphate receptor type 1 mRNA in neuronal dendrites. J Biol Chem,2004,17,279(51):53427-53434.
[2]Vercauteren FG, Clerens S, Roy L. Early dysregulation of hippocampal protein in transgenic rats with Alzheimer disease-linked mutations in amyloid precursor protein and presenilin 1.Brain Res Mol,2004 Dec 20,132(2):241-59.
[3]Gorg A, Obermaier C, Boguth G, et al. The current state of two-dimensional electrophoresis with immobilized PH gradients. Electrophoresis.2000,21:1037-1053.
[4]Decca MB, Bosc C, Luche S. Protein arginylation in rat brain cytosol:a proteomic analysis. Neurochem Res.2006 Mar;31(3):401-9.
[5]Hwang YY, Li MD.Proteins differentially expressed in response to nicotine in five rat brain regions:identification using a 2-DE/MS-based proteomics approach. proteomics.2006 May,6(10):31318-53.
[6]Reifschneider NH, Goto S, Nakamoto H. Defining the mitochondrial proteomes from five rat organs in a physiologically significant context using 2D blue-native/SDS-PAGE. J Proteome Res.2006 May,5(5):1117-32.
[7]Arrell DK, Elliott ST, Kane LA, et al. Proteomic analysis of pharmacological precondioning:novel protein targets converge to mitoehondrial metabolism pathways. Circ Res,2006,99(7):706-714.
[8]Guillon JM,Rochette L,Baranes H.Effects of Ginkgo biloba extract on two models of experimental myocardial ischemia. Presse Med,1986,15(31):1516.
[9]Tosaki A,Engel man DT,Pali T,et al.Ginkgo biloba extract (EGB761) improves posrischenic function in isolated preconditioned working rat heart. Coron Artery Dis,1994,5(5):443.
[10]潘晓岩.银杏叶提取物对离体大鼠心脏再灌注心律失常的影响.中国药理学通报,1998,14(3)：283-285.
[11]Sam Hanash. Disease proteomics. Nature,2003,422:226-232.
[12]Wulfkuhle JD, Paweletz CP, Steeg PS, et al. Proteomic approaches to the diagnosis, treatment, and monitoring of Cancer. Adv Exp Med Biol,2003,532:59-68.
[13]Page M, Amess B, Rohlff C, et al. Proteomics:a major new technology for the drug discovery process. Drug Discov Today,1999,4:55-62.
[14]Wang JH, Hewick RM. Proteomics in drug discovery. Drug Discov Today,1999,4:129-133.
[15]Molloy MP. Two dimensional electrophoresis of membrane proteins using immobilized pH gradients. Anal Biochem,2000,280:
[16]Klein E, Klein JB, Thongboonkerd V,et al. Two dimensionalgel electrophoresis:a fundamental tool for expression protemics studies.Conirib Nephrol,2004,141:25.
[17]Lim MS, Elenitoba-Johnson KS.Proteomics in pathology research.Lab Invest,2004,141:25.
[18]Tyers M, Mann M. From genomics to proteomics. Nature,2003,422 (6928): 193-197.
[19]Randall MD, Keon CA, Greenhaff PL et al. Dual effects of dichloroacetate on cardiac ischaemic preconditioning in the rat isolated perfused heart. Br J Pharmacol 1998;124(1):245-51.
[20]Saiki Y, Lopaschuk GD, Dodge K et al. Pyruvate augments mechanical function via activation of the pyruvate dehydrogenase complex in reperfused ischemic immature rabbit hearts. J Surg Res 1998;79(2):164-9.
[21]张振英,刘秀华,孙胜,等.腹主动脉狭窄致大鼠心肌肥大后心肌组织蛋白质组变化的研究.中国微循环,2009,13(2)：84-89.
[22]Fert-Bober J, Sawicki G, Lopaschuk GD et al. Proteomic analysis of cardiac metabolic enzymes in asphyxiated newborn piglets. Mol Cell Biochem,2008,318 (1-2):13-21.
[23]Popova T, Pinheiro de Carvalho MA, Matasova L et al. Regulation of mitochondrial NADP-isocitrate dehydrogenase in rat heart during ischemia. Mol Cell Biochem,2007,294(1-2):97-105.
[24]Ito H, Nakano A, Kinoshita M,et al. Pioglitazone,a peroxisome proliferator-activated receptor-gamma agonist,attenuates myocardial ischemia reperfusion injury in a rat model. Lab Invest,2003,83(12):17-15.
[25]Liu HR, Tao L, Gao E,et al. Anti-apoptotic effects of rosiglitazone in hypercholesterolemic rabbits subjected to myocardial ischemia and reperfusion. Cardiovasc Res,2004,62(1):135.
[26]Yue TL, Chen J, Bao W, et al. In vivo myocardial protection from ischemia reperfusion injury by the peroxisome prolife rat or-activated receptor-gamma agonist rosiglitazone.Circulation,2001,104(21):2588.
[27]Naito Y, Yoshikawa T. Thiazolidinediones:a new class of drugs for the therapy of ischemia-reperfusion injury. Drugs Today(Barc),2004,40(5):423.
[28]Duan DY, Liu LL, Bozeat N,et al. Functional role of anion channels in cardiac diseases. Acta Pharmacol Sin.2005 Mar;26(3):265-78.
[29]Chen H, Liu LL, Ye LL, Targeted inactivation of cystic fibrosis transmembrane conductance regulator chloride channel gene prevents ischemic preconditioning in isolated mouse heart. Circulation,2004,10,110(6):700-4
[30]Xiang SY, Ye LL, Duan LL, et al. Characterization of a critical role for CFTR chloride channels in cardioprotection against ischemia/reperfusion injury. Acta Pharmacol Sin,2011,32(6):824-33.
[31]Hume JR, Duan D, Collier ML, et al. Anion transport in heart. Physiol Rev.2000; 80:31-81.
[32]Ruiz PE, Ponce ZA, Schanne OF. Early action potential shortening in hypoxic hearts:role of chloride current(s) mediated by catecholamine release. J Mol Cell Cardiol.1996; 28:279-290.
[33]Barriere H, Poujeol C, Tauc M, et al. CFTR modulates programmed cell death by decreasing intracellular pH in Chinese hamster lung fibroblasts. Am J Physiol. 2001; 281:C810-C824.
[34]Valverde MA, Vazquez E, Munoz FJ, et al. Murine CFTR channel and its role in regulatory volume decrease of small intestine crypts. Cell Physiol Biochem.2000; 10:321-328.
[35]Jacquelyne A, Kazuo A, Morgan AR.Fluorometric assays for DNAtopoisomerases and topoisomerase-targeted drugs:quantitation of catalytic activity and DNA cleavage. Molecular Pharmacology,1991,40:495.
[36]Xiaojian W, Nan L, Bin L, et al.A novel Human PhosPhatidylethanolamine-binding protein resists Tumor Necrosis Factor-indueed apotosis by inhibiting mitogen-activated protein kinase pathway activation and phosphatidylethanolamine externalization.J Biol Chem,2004,279:45855-45864.
[37]Li P, Wang X, Li N, et al. Anti-apoptotic hPEBP4 silencing promotes TRAIL-induced apoptosis of human ovarian cancer cells by activating ERK and JNK pathways. Int J Mol Med,2006,18(3):505-510.
[1]Duan DY, Liu LL, Bozeat N,et al. Functional role of anion channels in cardiac diseases. Acta Pharmacol Sin.2005 Mar;26(3):265-78.
[2]Chen H, Liu LL, Ye LL, Targeted inactivation of cystic fibrosis transmembrane conductance regulator chloride channel gene prevents ischemic preconditioning in isolated mouse heart. Circulation,2004,10,110(6):700-4
[3]Xiang SY, Ye LL, Duan LL, et al. Characterization of a critical role for CFTR chloride channels in cardioprotection against ischemia/reperfusion injury. Acta Pharmacol Sin,2011,32(6):824-33.
[4]Hume JR, Duan D, Collier ML, et al. Anion transport in heart. Physiol Rev.2000; 80:31-81.
[5]Ruiz PE, Ponce ZA, Schanne OF. Early action potential shortening in hypoxic hearts:role of chloride current(s) mediated by catecholamine release. J Mol Cell Cardiol.1996; 28:279-290.
[6]Barriere H, Poujeol C, Tauc M, et al. CFTR modulates programmed cell death by decreasing intracellular pH in Chinese hamster lung fibroblasts. Am J Physiol. 2001; 281:C810-C824.
[7]Valverde MA, Vazquez E, Munoz FJ, et al. Murine CFTR channel and its role in regulatory volume decrease of small intestine crypts. Cell Physiol Biochem.2000; 10:321-328.
[1]. Jennings RB, Reimer KA. Factors involved in salvaging ischemic myocardium: effect of reperfusion of arterial blood[J]. Circulation,1983,68(2 Pt 2):Ⅰ25-36.
[2]. Braunwald E, Kloner RA. Myocardial reperfusion:a double-edged sword?[J]. J Clin Invest,1985,76(5):1713-9.
[3]. Kloner RA. Does reperfusion injury exist in humans?[J]. J Am Coll Cardiol, 1993,21(2):537-45.
[4]. Schafer C, Ladilov Y, Inserte J et al. Role of the reverse mode of the Na+/Ca2+ exchanger in reoxygenation-induced cardiomyocyte injury[J]. Cardiovasc Res, 2001,51(2):241-50.
[5]. Gumina RJ, Buerger E, Eickmeier C et al. Inhibition of the Na(+)/H(+) exchanger confers greater cardioprotection against 90 minutes of myocardial ischemia than ischemic preconditioning in dogs[J]. Circulation,1999,100(25):2519-26; discussion 469-72.
[6]. Zeymer U, Suryapranata H, Monassier JP et al. The Na(+)/H(+) exchange inhibitor eniporide as an adjunct to early reperfusion therapy for acute myocardial infarction. Results of the evaluation of the safety and cardioprotective effects of eniporide in acute myocardial infarction (ESCAMI) trial[J]. J Am Coll Cardiol, 2001,38(6):1644-50.
[7]. Garcia-Dorado D, Inserte J, Ruiz-Meana M et al. Gap junction uncoupler heptanol prevents cell-to-cell progression of hypercontracture and limits necrosis during myocardial reperfusion[J]. Circulation,1997,96(10):3579-86.
[8]. Schulz R, Gres P, Skyschally A et al. Ischemic preconditioning preserves connexin 43 phosphorylation during sustained ischemia in pig hearts in vivo[J]. FASEB J,2003,17(10):1355-7.
[9]. Zweier JL, Talukder MA. The role of oxidants and free radicals in reperfusion injury[J]. Cardiovasc Res,2006,70(2):181-90.
[10]. Akizuki S, Yoshida S, Chambers DE et al. Infarct size limitation by the xanthine oxidase inhibitor, allopurinol, in closed-chest dogs with small infarcts[J]. Cardiovasc Res,1985,19(11):686-92.
[11]. Uraizee A, Reimer KA, Murry CE et al. Failure of superoxide dismutase to limit size of myocardial infarction after 40 minutes of ischemia and 4 days of reperfusion in dogs[J]. Circulation,1987,75(6):1237-48.
[12]. Ishii H, Ichimiya S, Kanashiro M et al. Impact of a single intravenous administration of nicorandil before reperfusion in patients with ST-segment-elevation myocardial infarction[J]. Circulation,2005,112(9):1284-8.
[13]. Kitakaze M, Asakura M, Kim J et al. Human atrial natriuretic peptide and nicorandil as adjuncts to reperfusion treatment for acute myocardial infarction (J-WIND):two randomised trials[J]. Lancet,2007,370(9597):1483-93.
[14]. Liang F, Gao E, Tao L et al. Critical timing of L-arginine treatment in post-ischemic myocardial apoptosis-role of NOS isoforms[J]. Cardiovasc Res, 2004,62(3):568-77.
[15]. Garcia-Dorado D, Rodriguez-Sinovas A, Ruiz-Meana M et al. The end-effectors of preconditioning protection against myocardial cell death secondary to ischemia-reperfusion[J]. Cardiovasc Res,2006,70(2):274-85.
[16]. Bond JM, Herman B, Lemasters JJ. Protection by acidotic pH against anoxia/reoxygenation injury to rat neonatal cardiac myocytes[J]. Biochem Biophys Res Commun,1991,179(2):798-803.
[17]. Petzelbauer P, Zacharowski PA, Miyazaki Y et al. The fibrin-derived peptide Bbetal5-42 protects the myocardium against ischemia-reperfusion injury[J]. Nat Med,2005,11(3):298-304.
[18]. Armstrong PW, Granger CB, Adams PX et al. Pexelizumab for acute ST-elevation myocardial infarction in patients undergoing primary percutaneous coronary intervention:a randomized controlled trial[J]. JAMA,2007,297(1): 43-51.
[19]. Griffiths EJ, Halestrap AP. Mitochondrial non-specific pores remain closed during cardiac ischaemia, but open upon reperfusion[J]. Biochem J,1995,307 (Pt 1)(93-8.
[20]. Spisani S, Fabbri E, Muccinelli M et al. Inhibition of neutrophil responses by cyclosporin A. An insight into molecular mechanisms[J]. Rheumatology (Oxford), 2001,40(7):794-800.
[21]. Piot C, Croisille P, Staat P et al. Effect of cyclosporine on reperfusion injury in acute myocardial infarction[J]. N Engl J Med,2008,359(5):473-81.
[22]. Hausenloy DJ, Yellon DM. Reperfusion injury salvage kinase signalling:taking a RISK for cardioprotection[J]. Heart Fail Rev,2007,12(3-4):217-34.
[23]. Heusch G, Boengler K, Schulz R. Cardioprotection:nitric oxide, protein kinases, and mitochondria[J]. Circulation,2008,118(19):1915-9.
[24]. Daemen MA, van't Veer C, Denecker G et al. Inhibition of apoptosis induced by ischemia-reperfusion prevents inflammation[J]. J Clin Invest,1999,104(5):541-9.
[25]. Matsui Y, Takagi H, Qu X et al. Distinct roles of autophagy in the heart during ischemia and reperfusion:roles of AMP-activated protein kinase and Beclin 1 in mediating autophagy[J]. Circ Res,2007,100(6):914-22.
[26]. Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia:a delay of lethal cell injury in ischemic myocardium[J]. Circulation,1986,74(5):1124-36.
[27]. Kuzuya T, Hoshida S, Yamashita N et al. Delayed effects of sublethal ischemia on the acquisition of tolerance to ischemia[J]. Circ Res,1993,72(6):1293-9.
[28]. Liu GS, Thornton J, Van Winkle DM et al. Protection against infarction afforded by preconditioning is mediated by A1 adenosine receptors in rabbit heart[J]. Circulation,1991,84(1):350-6.
[29]. Ganote CE, Armstrong S, Downey JM. Adenosine and A1 selective agonists offer minimal protection against ischaemic injury to isolated rat cardiomyocytes[J]. Cardiovasc Res,1993,27(9):1670-6.
[30]. Yitzhaki S, Huang C, Liu W et al. Autophagy is required for preconditioning by the adenosine A1 receptor-selective agonist CCPA[J]. Basic Res Cardiol, 2009,104(2):157-67.
[31]. Hori M, Kitakaze M, Sato H et al. Staged reperfusion attenuates myocardial stunning in dogs. Role of transient acidosis during early reperfusion[J]. Circulation,1991,84(5):2135-45.
[32].Tong H, Bernstein D, Murphy E et al. The role of beta-adrenergic receptor signaling in cardioprotection[J]. FASEB J,2005,19(8):983-5.
[33]. Thornton JD, Daly JF, Cohen MV et al. Catecholamines can induce adenosine receptor-mediated protection of the myocardium but do not participate in ischemic preconditioning in the rabbit[J]. Circ Res,1993,73(4):649-55.
[34]. Kudej RK, Shen YT, Peppas AP et al. Obligatory role of cardiac nerves and alpha 1-adrenergic receptors for the second window of ischemic preconditioning in conscious pigs[J]. Circ Res,2006,99(11):1270-6.
[35]. Sanada S, Komuro I, Kitakaze M. Pathophysiology of myocardial reperfusion injury:preconditioning, postconditioning, and translational aspects of protective measures[J]. Am J Physiol Heart Circ Physiol,301(5):H1723-41.
[36]. Ytrehus K, Liu Y, Downey JM. Preconditioning protects ischemic rabbit heart by protein kinase C activation[J]. Am J Physiol,1994,266(3 Pt 2):H1145-52.
[37]. Sanada S, Asanuma H, Tsukamoto O et al. Protein kinase A as another mediator of ischemic preconditioning independent of protein kinase C[J]. Circulation, 2004,110(1):51-7.
[38]. Sivaraman V, Hausenloy DJ, Kolvekar S et al. The divergent roles of protein kinase C epsilon and delta in simulated ischaemia-reperfusion injury in human myocardium[J]. J Mol Cell Cardiol,2009,46(5):758-64.
[39]. Kitakaze M, Hori M. It is time to ask what adenosine can do for cardioprotection[J]. Heart Vessels,1998,13(5):211-28.
[40]. Saxena M, Williams S, Tasken K et al. Crosstalk between cAMP-dependent kinase and MAP kinase through a protein tyrosine phosphatase[J]. Nat Cell Biol, 1999,1(5):305-11.
[41]. Sanada S, Kitakaze M, Papst PJ et al. Cardioprotective effect afforded by transient exposure to phosphodiesterase Ⅲ inhibitors:the role of protein kinase A and p38 mitogen-activated protein kinase[J]. Circulation,2001,104(6):705-10.
[42]. Saurin AT, Martin JL, Heads RJ et al. The role of differential activation of p38-mitogen-activated protein kinase in preconditioned ventricular myocytes[J]. FASEB J,2000,14(14):2237-46.
[43]. Behrends M, Schulz R, Post H et al. Inconsistent relation of MAPK activation to infarct size reduction by ischemic preconditioning in pigs[J]. Am J Physiol Heart Circ Physiol,2000,279(3):H1111-9.
[44]. Boengler K, Buechert A, Heinen Y et al. Cardioprotection by ischemic postconditioning is lost in aged and STAT3-deficient mice[J]. Circ Res, 2008,102(1):131-5.
[45]. Cohen MV, Yang XM, Liu Y et al. Cardioprotective PKG-independent NO signaling at reperfusion[J]. Am J Physiol Heart Circ Physiol, 2010,299(6):H2028-36.
[46]. Sanada S, Node K, Asanuma H et al. Opening of the adenosine triphosphate-sensitive potassium channel attenuates cardiac remodeling induced by long-term inhibition of nitric oxide synthesis:role of 70-kDa S6 kinase and extracellular signal-regulated kinase[J]. J Am Coll Cardiol,2002,40(5):991-7.
[47]. Costa AD, Garlid KD. Intramitochondrial signaling:interactions among mitoKATP, PKCepsilon, ROS, and MPT[J]. Am J Physiol Heart Circ Physiol, 2008,295(2):H874-82.
[48]. Halestrap AP, Pasdois P. The role of the mitochondrial permeability transition pore in heart disease[J]. Biochim Biophys Acta,2009,1787(11):1402-15.
[49]. Halestrap AP. What is the mitochondrial permeability transition pore?[J]. J Mol Cell Cardiol,2009,46(6):821-31.
[50]. Ovize M, Baxter GF, Di Lisa F et al. Postconditioning and protection from reperfusion injury:where do we stand? Position paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology[J]. Cardiovasc Res,2010,87(3):406-23.
[51]. Manintveld OC, Te Lintel Hekkert M, van den Bos EJ et al. Cardiac effects of postconditioning depend critically on the duration of index ischemia[J]. Am J Physiol Heart Circ Physiol,2007,292(3):H1551-60.
[52]. Kharbanda RK, Mortensen UM, White PA et al. Transient limb ischemia induces remote ischemic preconditioning in vivo[J]. Circulation,2002,106(23):2881-3.
[53]. Przyklenk K, Bauer B, Ovize M et al. Regional ischemic 'preconditioning' protects remote virgin myocardium from subsequent sustained coronary occlusion[J]. Circulation,1993,87(3):893-9.
[54]. Birnbaum Y, Hale SL, Kloner RA. Ischemic preconditioning at a distance: reduction of myocardial infarct size by partial reduction of blood supply combined with rapid stimulation of the gastrocnemius muscle in the rabbit[J]. Circulation, 1997,96(5):1641-6.
[55]. Bartel DP. MicroRNAs:target recognition and regulatory functions[J]. Cell, 2009,136(2):215-33.
[56]. Eulalio A, Huntzinger E, Izaurralde E. Getting to the root of miRNA-mediated gene silencing[J]. Cell,2008,132(1):9-14.
[57]. Zhao Y, Ransom JF, Li A et al. Dysregulation of cardiogenesis, cardiac conduction, and cell cycle in mice lacking miRNA-1-2[J]. Cell, 2007,129(2):303-17.
[58]. Thum T, Galuppo P, Wolf C et al. MicroRNAs in the human heart:a clue to fetal gene reprogramming in heart failure[J]. Circulation,2007,116(3):258-67.
[59].Cordes KR, Srivastava D. MicroRNA regulation of cardiovascular development[J]. Circ Res,2009,104(6):724-32.
[60]. Fichtlscherer S, De Rosa S, Fox H et al. Circulating microRNAs in patients with coronary artery disease[J]. Circ Res,2010,107(5):677-84.
[61]. Tang Y, Zheng J, Sun Y et al. MicroRNA-1 regulates cardiomyocyte apoptosis by targeting Bcl-2[J]. Int Heart J,2009,50(3):377-87.
[62]. Xu C, Lu Y, Pan Z et al. The muscle-specific microRNAs miR-1 and miR-133 produce opposing effects on apoptosis by targeting HSP60, HSP70 and caspase-9 in cardiomyocytes[J]. J Cell Sci,2007,120(Pt 17):3045-52.
[63]. Wang Y, Lee CG. MicroRNA and cancer--focus on apoptosis[J]. J Cell Mol Med, 2009,13(1):12-23.
[64]. Ren XP, Wu J, Wang X et al. MicroRNA-320 is involved in the regulation of cardiac ischemia/reperfusion injury by targeting heat-shock protein 20[J]. Circulation,2009,119(17):2357-66.
[65]. Bonauer A, Carmona G, Iwasaki M et al. MicroRNA-92a controls angiogenesis and functional recovery of ischemic tissues in mice[J]. Science, 2009,324(5935):1710-3.
[66]. Wang S, Aurora AB, Johnson BA et al. The endothelial-specific microRNA miR-126 governs vascular integrity and angiogenesis[J]. Dev Cell, 2008,15(2):261-71.
[67]. Yin C, Salloum FN, Kukreja RC. A novel role of microRNA in late preconditioning:upregulation of endothelial nitric oxide synthase and heat shock protein 70[J]. Circ Res,2009,104(5):572-5.
[68]. Dong S, Cheng Y, Yang J et al. MicroRNA expression signature and the role of microRNA-21 in the early phase of acute myocardial infarction[J]. J Biol Chem, 2009,284(43):29514-25.
[69]. Sayed D, He M, Hong C et al. MicroRNA-21 is a downstream effector of AKT that mediates its antiapoptotic effects via suppression of Fas ligand[J]. J Biol Chem,2010,285(26):20281-90.
[70]. He L, Lemasters JJ. Heat shock suppresses the permeability transition in rat liver mitochondria[J]. J Biol Chem,2003,278(19):16755-60.
[71]. Ivan M, Haberberger T, Gervasi DC et al. Biochemical purification and pharmacological inhibition of a mammalian prolyl hydroxylase acting on hypoxia-inducible factor[J]. Proc Natl Acad Sci U S A,2002,99(21):13459-64.
[72]. Ockaili R, Natarajan R, Salloum F et al. HIF-1 activation attenuates postischemic myocardial injury:role for heme oxygenase-1 in modulating micro vascular chemokine generation[J]. Am J Physiol Heart Circ Physiol, 2005,289(2):H542-8.
[73]. Natarajan R, Salloum FN, Fisher BJ et al. Hypoxia inducible factor-1 activation by prolyl 4-hydroxylase-2 gene silencing attenuates myocardial ischemia reperfusion injury[J]. Circ Res,2006,98(1):133-40.
[74]. Rane S, He M, Sayed D et al. Downregulation of miR-199a derepresses hypoxia-inducible factor-1 alpha and Sirtuin 1 and recapitulates hypoxia preconditioning in cardiac myocytes[J]. Circ Res,2009,104(7):879-86.