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培哚普利对急性心肌梗死后大鼠心肌组织中AngⅡ、ERK1/2、c-fos mRNA含量的影响 被引量:3

Effects of perindopril on the content of AngⅡ,ERK 1/2 and c-fos mRNA in myocardial tissue after acute myocardial infarction in rats
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摘要 目的:探讨大鼠急性心肌梗死后心肌组织中AngⅡ、ERK1/2、c-fos mRNA含量的变化及培哚普利的干预作用。方法:结扎大鼠左冠状动脉前降支建立心肌梗死模型,随机分为心肌梗死组(A组,n=14)和培哚普利干预组(B组,n=14),另设假手术组为对照(C组,n=14)。术后24hB组给予培哚普利灌胃,A、C组给予蒸馏水灌胃,6周后处死,取心脏并计算左心室质量指数;分别采用放射免疫法、免疫组织化学法、实时荧光定量PCR法测定各组大鼠非梗死区心肌组织中AngⅡ含量、ERK1/2含量及原癌基因c-fos mRNA的含量。结果:6周后A、B组左心室质量指数、AngⅡ、ERK1/2及c-fos mRNA含量均较C组明显升高(P均<0.05);与A组相比,B组左心室质量指数、AngⅡ、ERK1/2及c-fos mRNA含量均明显下降(P均<0.05)。结论:培哚普利能降低AngⅡ,ERK1/2,c-fos mRNA的表达,改善左心室重塑。 Aim : To study the effects of perindopril on the content of Ang Ⅱ ,ERK 1/2 and c-fos mRNA in myocardial tissue after acute myocardial infarction in rats. Methods:After the model of myocardial infarction was established by ligating the left anterior descending artery of rats, the survivals were randomly divided into two groups : group A ( myocardial infarction group, n = 14) and group B (perindopril group, n = 14). Meanwhile, the other 14 sham-operated rats were used as control group( group C, n = 14). Each group was treated with direct gastric gavage from the second day, and rats of group B were treated with perindopril, group A and C ,with pure water. Six weeks later,the heart was havested, and the left ventricular weight index was calculated, the Ang Ⅱ content, the ERK1/2 content and the expression of c-fos mRNA were respectively detected with radioimmunoassay, immunohistocbemistry method and real-time fluorescent quantitative PCR. Resulits: Compared with group C, Ang Ⅱ , ERK1/2 content, expression of c-fos mRNA and left ventricular weight index significantly increased in group A and B (P 〈0.05 ). The above parameters in group B were lower than those in group A( P 〈 0.05). Conclusion:Perindopril can remarkably reduce the expression of c-fos mRNA and the content of Ang Ⅱ and ERK1/2 in myocardium,thus improve the ventricalar remodeling.
出处 《郑州大学学报(医学版)》 CAS 北大核心 2008年第1期146-149,共4页 Journal of Zhengzhou University(Medical Sciences)
关键词 心肌梗死 心室重塑 培哚普利 信号转导 大鼠 myocardial infarction ventricular remodeling perindopril singal transduction rat
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参考文献10

  • 1Lenormand P,Brondello JM,Brunet A,et al.Growth factor-induced p42/p44 MAPK nuclear translocation and retention requires both MAPK activation and neosynthesis of nuclear anchoring proteins[J].J Cell Biol,1998,142(3):625
  • 2Maisel A,Cesario D,Baird S,et al.Experimental autoimmune myocarditis produced by adoptive transfer of splenocytes after myocardial infarction[J].Circ Res,1998,82(4):458
  • 3Paul M,Ganten D.The molecular basis of cardiovascular hypertrophy:the role of he renin-angiotension sysrem[J].J Cardiovasc Pharmacol,1992,19 (Suppl 5):S51
  • 4Hefti MA,Harder BA,Eppenberger HM,et al.Signaling pathways in cardiac myocyte hypertroph[J].J Mol Cell Cardiol,1997,29(11):2 873
  • 5Sadoshima J,Izumo S.Signal transduction pathways of angiotensinⅡ-induced c-fos gene expression in cardiac myocytes in vitro.Roles of phospholipid-derived second messengers[J].Circ Res,1993,73(3):424
  • 6谈世进,潘敬运,詹澄扬,朱晓南.血管紧张素Ⅱ对培养心肌细胞c-fos表达和蛋白质合成的作用[J].生理学报,1999,51(5):521-526. 被引量:9
  • 7Moalic JM,Moazami-Goudarzi K,Thiem NV,et al.Hormonal induction of c-fos and HSP68 mRNAs on an isolated coronary perfused adult rat heart[J].Arch Int Physiol Biochim Biophys,1992,100(2):165
  • 8Bishopric NH,Jayasena V,Webster KA.Positive regulation of the skeletal alpha-actin gene by Fos and Jun in cardiac myocytes[J].J Biol Chem,1992,267(35):25 535
  • 9李爱萍,陈光辉,李天德,王友桂,李志敏,胡大一.不同水平干预对心肌细胞ERK核转位及c-fos表达的影响[J].中华内科杂志,2005,44(2):102-105. 被引量:10
  • 10Myerson SG,Montgomery HE,Whittingham M,et al.Left ventricular hypertrophy with exercise and ACE gene insertion/deletion polymorphism:a randomized controlled trial with Losarton[J].Circulation,2001,103(2):226

二级参考文献15

  • 1陈伟红,谭定定,潘敬运,胡本荣.血管紧张素Ⅱ诱导左心室原癌基因c-fos和c-myc的表达[J].生理学报,1995,47(1):59-64. 被引量:8
  • 2谭定定,钟春宁,陈伟红,潘敬运,胡本荣.压力超负荷诱导左心室原癌基因c-fos的表达[J].生理学报,1996,48(1):65-69. 被引量:5
  • 3Lenormand P, Brondello JM, Brunet A, et al. Growth factor-induced p42/p44 MAPK nuclear translocation and retention requires both MAPK activation and neosynthesis of nuclear anchoring proteins.J Cell Biol, 1998,142:625-633.
  • 4Simpson DG, Decker ML, Clark WA,et al. Contractile activity and cell-cell contact regulate myofibrillar organization in cultured cardiac myocytes. J Cell Bio1,1993,123:323-336.
  • 5Duff JL, Marrero MB, Paxton WG, et al. Angiotensin Ⅱ signal transduction and the mitogen-activated protein kinase pathway.Cardiovasc Res,1995,30:511-517.
  • 6Todisco A, Takeuchi Y, Yamada J, et al. Molecular mechanisms for somatostatin inhibition of c-fos gene expression. Am J Physiol, 1997,272(4 Pt 1) :G721-G726.
  • 7Pellieux C, Sauthier T, Aubert JF, et al. Angiotensin Ⅱ-induced cardiac hypertrophy is associated with different mitogen-activated protein kinase activation in normotensive and hypertensive mice.J Hypertens, 2000,18 : 1307-1317.
  • 8Lijnen P, Petrov V. Renin-angiotensin system, hypertrophy and gene expression in cardiac myocytes. J Mol Cell Cardiol, 1999,31 : 949-970.
  • 9Brunet A, Roux D, Lenormand P, et al. Nuclear translocation of p42/p44 mitogen-activated protein kinase is required for growth factor-induced gene expression and cell cycle entry. EMBO J, 1999,18:664-674.
  • 10Lee KH, Hajjar R.I, Matsui T, et al. Cardiac signal transduction.J Nucl Cardiol,2000,7:63-71.

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