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基质金属蛋白酶2及其抑制剂在大鼠心肌梗死后表达的变化 被引量:5

Matrix Metalloproteinases-2 and Tissue Inhibitor of Metalloproteinases-2 in Rat Cardiac Extracellular Matrix Remodeling after Acute Myocardial Infarction
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摘要 目的 为探讨基质金属蛋白酶2及其抑制剂在心肌梗死后慢性心力衰竭大鼠心室重塑过程中的作用。方法 大鼠随机分为心肌梗死组及假手术对照组,采用免疫组织化学法和免疫印迹法检测心肌基质金属蛋白酶2及其抑制剂的表达水平。结果 梗死后心肌基质金属蛋白酶2表达持续增加,其抑制剂表达也增加且以梗死后早期为主:梗死后1周时表达最强,1月后其表达明显减弱。Western印迹结果发现,基质金属蛋白酶2在心肌梗死后表达明显增加,其抑制剂表达也增加且以梗死后早期为主。结论 从与时间相关性来看,梗死后时间越长,心功能越差,基质金属蛋白酶相对含量越高,而其抑制剂表达则随梗死时间延长而减弱。 Aim To observe the role of matrix metalloproteinase-2(MMP-2) and tissue inhibitor of metalloproteinases-2(TIMP-2) on the left ventricular function and extracellular matrix remodeling after acute myocardial infarction. Methods Male SD rats were randomly divided into operator group and sham group, and the model was established by ligation of coronary artery. The left ventricular function (by catheter measuring) were studied at different time. The protein expression of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinases-2 was examined by immunohistochemical analysis and Western-blot. Results Compared with sham group, the left ventricular function deteriorated and ventricular remodeling occurred after acute myocardial infarction. And the protein expression of matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 elevated (P<0.05). Conclusion Matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-2 involved in the left ventricular function deterioration and ventricular remodeling after acute myocardial infarction.
出处 《中国动脉硬化杂志》 CAS CSCD 2005年第2期189-191,共3页 Chinese Journal of Arteriosclerosis
关键词 病理学与病理生理学 基质金属蛋白酶2 基质金属蛋白酶抑制剂 免疫印迹法 心肌梗死 心力衰竭 心室重构 Matrix Metalloproteinase Tissue Inhibitor of Metalloproteinases Immunohistochemical Analysis Myocardial Infarction Heart Failure Ventricular Remodeling Western Blot
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  • 1Whittaker P,Boughner DR,Kloner RA.Role of collagen in acute myocardial infarct expansion.Circulation,1991,84:2 123-26.
  • 2Kim HE,DalalSS,Young E,Legato MJ,Weisfeldt ML,D'Armiento J.Disruption of the myocardial extracellular matrix leads to cardiac dysfunction.J Clin Invest,2000,106:857-859.
  • 3Jugdll BI,Kban MI,Jugdull SJ,Tian L.Effect of prolonged inotropic stimulation on ventricular remodeling during healing after myocardial infarction in the dog:mechanistic insights.JACC,1996,27:1 787-792.
  • 4Cleutjens JP,kandala JC,Guarda E,Guntaka RV,Weber KT.Regulation of collagen degradation in the rat myocardium after infarction.J Mol Cell Cardiol,1995,27:1 281-285.
  • 5Sun Y,Zhang JQ,Zhang J.Cardiac remodeling by fibrous tissueafter infarction in rats.J Lab Clin Med,2000,135:316-320.
  • 6Iwanaga Y,Aoyama T,Kihara Y,Onozawa Y,Yoneda T,Sasayama S.Excessive activation of matrix metalloproteinases coincides with left ventricular remodeling during transition from hypertrophy to heart failure in hypertensive rats.J Am Coll Cardiol,2002,39:1 384-387.
  • 7Creemers EE,Davis JN,Parkhurst AM,Leenders P,Dondy KB,Hapke E.Difficiency of tissue inhibitor of matrix metalloproteinase lexacerbates LV remodeling following myocardial infarction in mice.Am J Physiol Heart Circ Physiol,2003,284(1):H364-371.
  • 8Fedak PW,Altamentova SM,Weisel RD,Nili N,Ohno N,Verma S.Matrix remodeling in human heart failure:a possible regulatory role for TIMP-3.Am J Physiol Heart Circ Physiol,2003,284(2):H626-634.

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