我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

大鼠心肌梗死后心肌NF-κB、 MMP-2和TIM-2表达变化及其意义(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第1期
页码:
54-56，59
栏目:
基础研究
出版日期:
2006-01-01

文章信息/Info

Title:
Expression of NF-κB, metalloproteinases and tissue inhibitor of metalloproteinases in rat ventricular remodeling after acute myocardial infarction
作者:
张军;  贾国良 ; 王海昌 ; 郭文怡
第四军医大学西京医院心内科，陕西 西安 710032
Author(s):
ZHANG Jun;  JIA Guo-liang;  WANG Hai-chang;  GUO Wen-yi
Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi’an，Shaanxi, 710032，China
关键词:
心肌梗塞; 心室重构; 核转录因子; 基质金属蛋白酶; 基质金属蛋白酶抑制物
Keywords:
myocardial infarction;  ventricular remodeling;  nuclear factor kappa B;  metalloproteinase;  tissue inhibitor of metalloproteinases
分类号:
R542.22
DOI:
-
文献标识码:
A
摘要:
目的 探讨心肌梗死（MI）后大鼠心肌NF-κB、 MMP-2和TIMP-2表达变化及其在心室重构和心力衰竭的病理意义。方法结扎冠状动脉左前降支复制大鼠心肌梗死模型。术后24 h将存活大鼠随机分为MI组及假手术（SH）组。采用免疫组化法及免疫印迹法观察MMP-2和TIMP-2在MI后不同时间点的表达变化，采用凝胶电泳迁移率变化法分析NFκB活性变化。结果MI后NF-κB活性明显增强，在心肌细胞中表达呈阳性。MI后心肌MMP-2、TIMP-2表达均增加。从时间的相关性看，MI后时间越长，心功能越差，MMP-2相对含量越高，而TIMP-2表达则随梗死时间延长而减弱。结论大鼠MI后心肌组织中NF-κB活性和 MMP-2、TIMP-2表达水平都发生了明显变化，可能参与了MI后心室重构的病理过程。
Abstract:
AIM To observe changes of expression of NF-κB, metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinases-2 (TIMP-2) during ventricular remodeling following acute myocardial infarction and to investigate its pathological significance. METHODS The myocardial infarction model was established on rats by ligation of coronary artery. Twenty four hours after the operation, rats were randomly divided into operation group and sham group. The protein expressions of MMP-2 and TIMP-2 were examined by immunohistochemical analysis and Westernblot. The change of NFκB activity was analyzed by EMSA. RESULTS The activity of NFκB was enhanced after myocardial infarction and the expressions of MMP-2 and TIMP-2 were elevated(P<0 .0 5 ) . CONCLUSION NF-κB activity and expressions of MMP-2 and TIMP-2 change significantly after myocardial infarction, suggesting that all the three factors maybe involved in ventricular remodeling following acute myocardial infarction.

参考文献/References

［1］戴闺柱.慢性心力衰竭治疗的现代概念［J］.中华心血管病杂志,2000,28(1):75-78.

［2］ Kim HE, Dalal SS, Young E, et al. Disruption of the myocardial extracellular matrix leads to cardiac dysfunction［J］. J Clin Invest, 2000, 106:857.

［3］冷启新，刘执玉，李瑞祥,等. NF-κB抑制剂对THP-1粘附及MMP-9表达影响的实验研究［J］. 解剖科学进展,2000,6(4): 363-365.

［4］Jugdll BI, Kban MI, Jugdull SJ, et al. Effect of prolonged inotropic stimulation on ventricular remodeling during healing after myocardial infarction in the dog: mechanistic insights［J］. JACC, 1996,27:1787.

［5］汪永义，薛松，萧明第，等. NFκB激活在大鼠心肌细胞缺血再灌注损伤中的意义［J］.中国胸心血管外科临床杂志,2004,11(2):127－130.

［6］李小丛. 核转录因子kappa B与心肌缺血再灌注损伤［J］. 国外医学·麻醉学与复苏分册， 2001，22（5）：288－290.

［7］Parodi FE, Mao D, Ennis TL, et al. Suppression of experimental abdominal aortic aneurysms in mice by treatment with pyrrolidine dithiocarbamate, an antioxidant inhibitor of nuclear factorκB［J］ . J Vasc Surg， 2005,41:479-489.

［8］Jones WK, Brown M, Ren X,et al. NFκB as an integrator of diverse signaling pathways: The heart of myocardial signaling［J］. Cardiovasc Toxicol， 2003, 3(3):229-254.

［9］Upchurch GR, Welch GN, Fabian AJ, et al. Homocyst(e)ine decreases bioavailable nitric oxide by a mechanism involving glutathione peroxidase［J］. J Biol Chem,1997,272:17012-17017.

［10］张怀勤，张恩光，徐力辛，等. 基质金属蛋白酶对大鼠心肌梗死后心室重塑的影响［J］. 中华心血管病杂志，2003, 31(3):223－225.

［11］Mann DL, Spinale FG. Activation of matrix metalloproteinases in the failing human heart:breaking the ties that binds［J］. Circulation, 1998,97:1699-1702.

备注/Memo

备注/Memo:
收稿日期：2005-06-01.作者简介：张军，主治医师Tel：（029）84775183 Email：zhangch@fmmu.edu.cn
更新日期/Last Update: