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ERK1/2在慢性冬眠心肌中变化及意义的实验研究 被引量:5

ERK1/2在慢性冬眠心肌中变化及意义的实验研究
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摘要 目的 探讨慢性冬眠心肌(chronic hibernating myocardium,CHM)组织中胞外信号调节蛋白激酶(extracellular-signal regulated kinase,ERK1/2)的蛋白表达及其磷酸化形式(p-ERK1/2)的变化和意义。方法 10只小型中国家猪随机分为实验组(EXP,n=6)与对照组(CON,n=4)。实验组以右冠状动脉为靶血管,经右股动脉送入自制的缩窄器后继续喂养一个月制备成慢性冬眠心肌的模型。处死动物前三天采用硝酸甘油介入^(99)Tc^m-MIBI(^(99)锝~m-甲氧基异丙基丙腈)心肌灌注显像(SPECT)方法检测慢性冬眠心肌,获取对照组心肌组织(CON)、实验组中的正常心肌组织(NM)及慢性冬眠心肌组织(CHM)的样本进行光镜、电镜检查。采用免疫印迹(Western blotting)分析三组心肌组织中ERE1/2的蛋白表达及p-ERK1/2的变化。结果CHM中p-ERK1/2明显增高,与NM、CON中p-ERK1/2相比较有显著性差异(p<0.05,p<0.01)。结论 慢性冬眠心肌组织中ERK1/2被激活。 Objective To investigate the variation and significance of the member of mitogen-activated protein kinase ( MAP Kinase) superfamily-extracellular signal regulated kinase ( ERK1/2) and phosphorylated ERK1/2 (p-ERK1/2) in pig's chronic hibernating myocardium(CHM). Methods 10 little domestic Chinese pigs were divided into experiment group(n-6,EXP) and control group(n= 4,CON) by random. The constrictors were sent into right coronary arteries of animals of experiment group and the animals were feed one month to establish an animal model of CHM. Dectecting CHM by nitroglycerion ^99TC^m-MIBI SPECT( single-photo emission computed tomography)three days before the animals were killed. Verification the accuracy by observing the samples of CHM under microscope and electron microscope. Assessing the variation of ERK, p-ERK in nomal myocardium (NM), CHM, and CON by Western blotting. RESULT p-ERK 1/2 were significantly increased in CHM compared with NM and CON ( p 〈 0.05, p 〈 0.01 ) . CONCLUSION ERK were activated in tissues of CHM.
出处 《中国分子心脏病学杂志》 CAS 2003年第1期28-31,共4页 Molecular Cardiology of China
基金 江苏省应用基础研究项目BJ2000059
关键词 慢性冬眠心肌 ERK1/2 超微结构 Chronic hibernating myocardium extracellular signal regulated kinase(ERK1/2)Ultrastructure
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参考文献11

  • 1[1]Schulman D, Latchman DS, Yellon DM. Urocortin protects the heart from reperfusion injury via upregulation of p42/p44 MAPK signaling pathway. Am J Physiol Heart Circ Physiol 2002,283(4): H1481-8
  • 2[2]Buehler A, Martire A, Strohm C, et al. Angiogenesis-independent cardioprotection on FGF-1 transgenic mice. Cardiovasc Res 2002,55 (4): 768-77
  • 3郭庆林,孙立军.犬冠脉内狭窄模型闭胸制备技术:初步报告[J].临床医学影像杂志,1995,6(2):95-95. 被引量:4
  • 4[5]Miroslav Barancik, Patrik Htun, Wolfgang Schaper. Okadaic acid and anisomycin are pretective and stimulate the SAPK/JNK pathway. Journal of Cardiovascular Pharmacology. 1999,34:182-190
  • 5[6]Lowry DH, Rosebrough HJ, Rarr AL. Protein measurement with folin phenol reagent. J Biol Chem 1951,193:265-275
  • 6[7]Laemmli UK. Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature. 1970,227(259):680-5
  • 7[8]Towbin H, Staehelin T, Gordon J. Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets: procedure and some applications. Proc Natl Acad Sci U S A. 1979,76 (9) :4350-4
  • 8[9]Albrecht E, Martin S, Wolf-Peter, K et al. Hibernating Myocardium An Incomplete Adaptation to Ischemia. Circulation,1997,96: 2920-2931
  • 9[10]Suzuki A, Iwasali M,Kato M, et al. Sequential operation of ceramide synthesis and ICE cascade in CPT-11-initiated apoptotic death signaling. Exp Cell Res, 1997,233:41-47
  • 10刘秀华,杨军,王士雯,高雪,庞永政,唐朝枢.丝裂素活化蛋白激酶在大鼠心脏缺血预处理中的作用[J].中华医学杂志,1999,79(7):542-545. 被引量:11

二级参考文献12

  • 1李田昌 庞永政 等.丝裂素活化蛋白酶活性测定[J].基础医学与临床,1996,16:78-80.
  • 2刘秀华,基础医学与临床,1998年,18卷,3期,233页
  • 3Weinbrenner C,J Mol Cell Cardiol,1997年,29卷,2383页
  • 4刘秀华,生理科学进展,1997年,28卷,355页
  • 5于文杰,生理学报,1997年,45卷,531页
  • 6张钧华,中华心血管病杂志,1997年,25卷,215页
  • 7Maulik N,FEBS Lett,1996年,396卷,233页
  • 8李田昌,基础医学与临床,1996年,16卷,78页
  • 9张钧华,陈魁,陈健,刘秀华,叶赤,庞永政,汪丽蕙,唐朝枢.丝裂素活化蛋白激酶参与缺血预适应的延迟保护作用[J].中华心血管病杂志,1997,25(3):215-218. 被引量:13
  • 10刘秀华.缺血(氧)预处理的普遍性及临床应用前景[J].生理科学进展,1997,28(4):355-358. 被引量:9

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  • 1李东野,钱文浩,於江泉,夏勇,潘德锋,孙全胜,张中明.冠心病患者冬眠心肌中TNF-α表达及细胞凋亡的临床研究[J].徐州医学院学报,2007,27(3):148-151. 被引量:3
  • 2孙忠东,池一凡,夏家红,杨铁南,侯文明,杨辰垣.金属硫蛋白对供心细胞凋亡的影响[J].中国胸心血管外科临床杂志,2004,11(4):273-275. 被引量:2
  • 3管欣,刘中民,范慧敏,刘泳,陈国涵,徐志龙.缺氧过程中DADLE对心肌收缩力和收缩长度的影响[J].中国胸心血管外科临床杂志,2006,13(6):440-441. 被引量:1
  • 4钱文浩 於江泉 李东野 等.GLUT4、TNF-α-mRNA、iNOS在冠心病患者冬眠心肌中的表达及意义.中国心血管病研究杂志,:94-96.
  • 5Johnson GL, Lapadat R. Mitogen activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases[J]. Science,2002, 298(5600) : 1911-1912.
  • 6Robert DL, Byron JK,Gentian K, et al. Delayed adenosine A1 receptor preconditioning in rat myocardium is MAPK dependent but iNOS independent[J]. Am J Physiol Heart Cire Physiol 2005, 289:H785-H791.
  • 7Chen YR, TanTH. The c-Jun N-terminal kinase pathway and apoptotic signaling(review) [J]. Int J Oncol,2000,16(4):651- 662.
  • 8Omura T, Yoshiyama M, Yoshida K. Dominat negative mutant of c-Jun Inhibits cardiomyocyte hypertrophy induced by endothelin 1 and phenylephrine[J]. Hypertension, 201)2,39 ( 1 ) : 81- 86.
  • 9Iwai-Kanai E, Hasegawa K, Sawamura T, et al. Activation of lectin like oxidized low density lipoprotein receptor 1 induces apoptosis incultured neonatal rat cardiac myocytes[J]. Circulation, 2001,104: 2948-2954.
  • 10Zhao TC, Taher MM, Valerie KC. P38 Triggers late preconditioning elicited by anisomycin in heart; involvement of NF-kap paB and iNOS[J] . Circ Res, 2001,89(10):915-922.

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