期刊文献+

卡托普利对高血压心脏钙调蛋白磷酸酶与核因子κBp65蛋白表达的影响 被引量:1

Effects of captopril on expression of calcineurin and NF-κB p65 in the heart of hypertensive rats
下载PDF
导出
摘要 目的:探讨卡托普利对高血压大鼠心脏钙调蛋白磷酸酶(calcineurin)、核因子κBp65(NFκBp65)蛋白表达影响及其机制。方法:建立腹主动脉缩窄高血压大鼠模型,术后1周用卡托普利治疗,连续10周。以尾动脉测压法观察血压变化,用免疫组织化学和形态计量学方法,观察calcineurin、NF-κBp65在心脏表达和心脏系数的变化。结果:经卡托普利治疗,高血压大鼠血压降低(mmHg,P<0.01),心脏系数显著减小(g/100g,P<0.01),心脏calcineurin和NF-κBp65蛋白高表达下调,阳性表达面积和面积百分比缩小(μm2,P<0.01,或P<0.01)。结论:卡托普利能通过调控信号转导通路calcineurin-NFAT-NF-κBp65关键蛋白表达,逆转高血压心血管重构。 AIM: To study the effect of captopril on ealcineurin and NF - κB p65 in the signal transduction pathway of the cardiovascular remodeling in hypertensive rats. METHODS: Using a animal model of hypertension induced by abdominal aortic banding, the mrs were treated with captopril for 10 weeks. The blood pressure was observed with a tail cuff method. The heart weight and heart weight/body weight were measured. The expression of caleineurin and NF - κB p65 were studied by using immunohistochemistry. RESULTS: After treated with captopril, the blood pressure of the model rats was decreased (P 〈0. 01 ), the heart weight or heart weight/body weight were also decreased (P 〈0. 01 ). The calci- neurin and NF - κB p65 protein overexpression was down - regulated, NF - κB - positive area and area percentage were reduced in the heart of hypertensive rats (P 〈0. 01 ,P 〈0. 01 ). CONCLUSION: Captopril reverses the cardiovascular remodeling by affecting the overexpression of calcineurin and NF - κB p65 involved in the cardiovascular remodeling in hypertensive rats.
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2007年第1期40-43,共4页 Chinese Journal of Pathophysiology
基金 国家重点研究发展计划(973计划)基金资助项目(No.TG2000056901)
关键词 高血压 钙调蛋白磷酸酶 NF—κB 卡托普利 信号转导 Hypertension Calcineurin NF - kappa B Captopril Signal transduction
  • 相关文献

参考文献12

  • 1Jin H, Yang R, Awad TA, et al. Effects of early angiotensin- converting enzyme inhibition on cardiac gene expression after acute myocardial infarction[ J ]. Circulation,2001,103(5) : 736 -742.
  • 2Zou Y, Hiroi Y, Uozumi H. Calcineurin plays a critical role in the development of pressure overload - induced cardiac hypertrophy[J]. Circulation, 2001, 104( 1 ) : 97 -101.
  • 3Mano A, Tatsumi T, Shiraishi J. Aldosterone directly induces myocyte apoptosis through calcineurin dependent pathways[J]. Circulation, 2004, 110(3): 317-323.
  • 4苏兴利,高广道,罗秀成,王佐贤,王新凤,刘进军,林元喜.大鼠压力负荷性肥大心肌中TNF-αmRNA表达变化[J].中国病理生理杂志,2004,20(8):1414-1417. 被引量:4
  • 5Diedrichs H, Chi M, Boelck B. Increased regulatory activity of the calcineurin/NFAT pathway in human heart failure[J]. EurJ Heart Fail, 2004, 6(1): 3-9.
  • 6Frantz S, Stoerk S, Ok S. Effect of chronic heart failure on nuclear factor kappa B in peripheral leukocytes [ J ].Am J Cardiol, 2004, 94(5) : 671 -673.
  • 7Wilkins BJ, Dai YS, Bueno OF. Calcineurin/NFAT coupling participates in pathological, but not physiological,cardiac hypertrophy[J]. Circ Res, 2004, 94(1) : 110-118.
  • 8Fiedler B, Wollert KC. Interference of antihypertrophic molecules and signaling pathways with the Ca^2+ - calcineurin - NFAT cascade in cardiac myocytes [ J ]. Cardiovasc Res, 2004, 63(3) : 450 -457.
  • 9Jones WK, Brown M, Ben X. NF- kappa B as an integrator of diverse signaling pathways: the heart of myocardial signaling? [J]. Cardiovasc Toxicol, 2003, 3 (3) : 229-254.
  • 10Li Y, Ha T, Gao X. NF - kappa B activation is required for the development of cardiac hypertrophy in vivo [ J ]. Am J Physiol, 2004, 287(4): H1712- H1720.

二级参考文献13

  • 1田斌,高广道,曹治平,卢兴.血管紧张素Ⅱ刺激肥大心肌细胞和心肌成纤维细胞核酸蛋白质及胶原合成[J].中国病理生理杂志,1995,11(5):450-454. 被引量:13
  • 2Levine B, Kalman J, Mayer L, et al. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure[J]. N Engl J Med, 1990, 323(4) :236- 241.
  • 3Hirsch AT, Talsness CE, SmithAD, etal. Differentialeffects of captopril and enalapril on tissue renin- angiotension systems in experimental heart failure[J]. Circulation, 1992, 86(2): 1566 - 1574.
  • 4Bryant D, Becker L, Richardson J, et al. Cardiac failure in transgenic mice with myocardial expression of tumor necrosis factor- alpha[J]. Circulation, 1998, 97(14): 1375 - 1381.
  • 5Stamm C, Friens I, Cowan DB, et al. Inhibition of tumor necrosis factor- alpha improves postischemic recovery of hypertrophied hearts[J]. Circulation, 2001, 104( 12 suppl 1 ):I350- I355.
  • 6Kapadia SR, Yakoob K, Nader S, et al. Elevated circulating levels of serum tumor necrosis factor- alpha in patients with hemodynamically significant pressure and volume overload[ J].J Am Coll Cardiol, 2000, 36(1):208-212.
  • 7Fucuzawa M, Saton J, Sagara M, et al. Angiotension converting enzyme inhibitors suppress production of tumor necrosis factor- alpha in vitro and in vivo [ J ]. Immunophamacology,1997, 36(1):49-55.
  • 8Higuchi Y, Otsu K, Nishida K, et al. Involvement of reactive oxygen species- mediated NFκB activation in TNF- α induced cardiomyocyte hypertrophy [ J ]. Hypertension, 2002,34(2) :233 - 240.
  • 9Bogoyevitch MA, Andersson MB, Gillespie- brown J, et al.Adrenergic receptor stimulation of the mitogen- activated protein kinase cascade and cardiac hypertrophy[J]. Biochen J,1996, 314(Pt1) :115 - 121.
  • 10Horton JW, Maass D, White J, et al. Nitric oxide modulation of TNF- alpha- induced cardiac contractile dysfunction is concentration dependent[J]. Am J Physiol, 2000, 278(6):H1955 - H1965.

共引文献3

同被引文献4

引证文献1

二级引证文献3

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