期刊文献+

雷米普利诱导大鼠延迟相心脏保护作用及蛋白质组学研究 被引量:7

Delayed cardioprotection and differentiation of proteins expression induced by ramipril in rats
下载PDF
导出
摘要 目的 :研究雷米普利延迟相药理性预适应心脏保护作用 ,及其对心肌组织蛋白表达的影响。方法 :雄性Wistar大鼠分为2组 ,分别用生理盐水 (NS组 )和雷米普利 (1mg/kg) (RAM组 )灌胃 ,24h后冠脉左前降支行30min缺血/2h再灌注。观察缺血/再灌注期间心率、血压、心电图ST -段变化 ,记录室性心律失常的发生情况。测定麻醉后及再灌注2h血浆肌酸激酶水平。再灌注2h行心肌HE染色和TTC染色 ,定性和定量测定心肌梗死情况。每组各2只大鼠于预处理后24h取心室肌组织进行蛋白质组学研究。结果 :与NS组比较 ,RAM组缺血期ST -段抬高幅度明显降低 (P<0.01) ,室早、室速出现时间推迟 (P<0.001) ,持续时间缩短 (P<0.001) ,室颤发生率降低 (P<0.001) ,再灌注2h血浆肌酸激酶升高的程度降低 (P<0.05) ,心肌梗死范围缩小 (P<0.001)。双向电泳及凝胶染色后 ,对表达有显著性变化的12个蛋白点进行质谱分析 ,初步鉴定RAM组一种未命名蛋白表达增加。结论 :雷米普利在大鼠整体模型诱导延迟相心脏保护作用 。 Objective:To determine whether ramipril induces delayed cardioprotection against ischemia-reperfusion injury in rat in vivo and to examine protein expression in cardic tissue using the technique of proteomics.Methods:Rats were pretreated with normal saline(group NS)or ramipril(1mg/kg)(group RAM).Twenty-four hours later,all rats were subjected to30min coronary occlusion followed by2h reperfusion.The shift of ST segment and the episode of ventricular arrhythmias were monitored;the activity of creatine kinase(CK)in plasma,the infarct size and the protein expression were examined.Results:Compared with group NS,ramipril increased the tolerance of the heart to I/R injury:the elevation of ST-segment during ischemia was decreased(P<0.01),the onsets of ventricular premature contraction(VPC)and ventricular tachycardia(VT)were delayed(P<0.001),the durations of VPC and VT were shortened(P<0.001)and the incidence of ventricular fibrillation was decreased(P<0.001)remarkably.The concentration of CK in plasma corresponding to reperfusion(P<0.05)and myocardial infarct size was reduced(P<0.001)significantly as well.Twelve protein spots with significant changes in their expression were analyzed by mass spectrometry.The peptide fingerprint showed that an unnamed protein overexpressed in group RAM.Conclusion:The results indicate,for the first time,that pretreatment with ramipril24h before lethal ischemia induce delayed cardioprotection and an overexpression of an unnamed protein in rat.
出处 《天津医科大学学报》 2004年第1期5-10,共6页 Journal of Tianjin Medical University
基金 天津市科委自然科学基金资助项目 (项目编号 :003606811)
关键词 药理性预适应 延迟相心脏保护作用 雷米普利 蛋白质组学 Pharmacological preconditioning Delayed cardioprotection Ramipril Proˉteomics
  • 相关文献

参考文献15

  • 1Nozawa Y, Miura T, Tsuchida A, et al. Chronic treament with an ACEinhibitor, temocapril, lowers the threshold for the infarct size-limiting effect of ischemic preconditioning [J]. Cardiovasc Drugs Ther, 1999, 13(2): 151 被引量:1
  • 2Nayeem MA, Matherne GP, Mustafa SJ. Ischemic and pharmacological preconditioning induces further delayed protection in transgenic mouse cardiac myocytes over-expressing adenosine A(1) receptors(A(1) AR): role of A(1) AR, iNOS and K(ATP) channels [J]. Naun 被引量:1
  • 3Bolli R. Late phase of preconditioning[J]. Circ Res, 2000, 87(1): 972 被引量:1
  • 4Jin Z-Q, Chen X. Ramipril-induced delayed myocardial protection against free radical injury involves bradykinin B2receptor-NO pathway and protein synthesis[J]. British J Pharmacol, 1998, 125(3): 556 被引量:1
  • 5Jaberansari MT, Baxter GF, Muller CA, et al. Angiotensinconverting enzyme inhibition enhances a subthreshold stimulus to elicit delayed preconditioning in pig myocardium[J]. J Am Coll Cardiol, 2001, 37(7): 1996 被引量:1
  • 6Zhu BQ, Sun YP, Sievers RE, Comparative effects of pretreatment with captopril and losartan on cardiovascular protection in a rat model of ischemia-reperfusion[J]. J Am Coll Cardiol, 2000, 35(3): 787 被引量:1
  • 7Lazar HL, Bao Y, Rivers S, et al. Pretreatment with angiotensin-converting enzyme inhibitors attenuates ischmiareperfusion injury[J]. Ann Thorac Surg, 2002, 73(5): 1522 被引量:1
  • 8Patel HH, Fryer RM, Gross ER, et al. 12-lipoxygenase in opioid-induced delayed cardioprotection: gene array, mass spectrometric, and pharmacological analyses[J].Circ Res,2003, 92(6): 676 被引量:1
  • 9Tang XL, Kodani E, Takano H, et al. Protein tyrosine kinase signaling is necessary for NO donor-induced late preconditioning against myocardial stunning[J]. Am J Physiol Heart Circ Physiol, 2003, 284(4): H1441 被引量:1
  • 10Laode K, Favre J, Thuillez C, et al. NO produced by endothelial NO synthase is a mediator of delayed preconditioning-induced endothelial protection[J]. Am J Physiol Heart Circ Physiol, 2003, 284(6): H2053 被引量:1

同被引文献88

引证文献7

二级引证文献29

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部