期刊文献+

MMP-3、TIMP-1、NO水平与川崎病冠脉损害的关系研究

RELATIONSHIP OF MMP-3、TIMP-1 AND NO LEVELS WITH CORONARY ARTERY LESION IN KAWASAKI DISEASE
下载PDF
导出
摘要 目的:研究川崎病(KD)患儿血清基质金属蛋白酶3(MMP-3)、基质金属蛋白酶抑制剂1(TIMP-1)及一氧化氮(NO)的表达水平,探讨其在KD冠脉损害中的作用。方法:用固相夹心法酶联免疫吸附实验(ELISA)测定各组患儿血清中MMP-3、TIMP-1的水平,用硝酸还原法检测各组患儿血清中NO的水平。结果:川崎病CAL组血清MMP-3、MMP-3/TIMP-1与NCAL组相比明显升高(P<0.05);血清TIMP-1水平较NCAL组明显降低(P<0.01);KD急性期和恢复期MMP-3、TIMP-1、MMP-3/TIMP-1水平与正常对照组相比较均明显升高(均P<0.01)。川崎病CAL组NO水平明显高于NCAL组(P<0.05);血清MMP-3与NO之间呈显著正相关(r=0.898,P<0.01);血清中TIMP-1与NO之间呈显著负相关(r=-0.772,P<0.01)。结论:川崎病CAL组血清MMP-3和NCAL组相比明显升高,提示MMP-3可以作为KD伴发冠脉损害的血生化指标之一。KD急性期MMP-3、TIMP-1、MMP-3/TIMP-1水平明显高于恢复期和对照组,提示MMP-3、TIMP-1、MMP-3/TIMP-1可作为早期诊断川崎病的一个客观生化指标。NO过度表达参与了KD急性期冠脉损害的发生发展,可以将循环中NO水平作为判断KD冠脉损害的一个有效指标。 Objective:To explore the expression of MMP-3,TIMP-1 and NO in Kawasaki disease,and discuss their expression in the coronary artery lesion(CAL)with KD.Methods:The serum levels of MMP-3,TIMP-1,were detected by Enzyme-linked immunosorbent assay(ELISA).The serum level of NO was measured by nitrate reductase spectrophotometry.Results:MMP-3 and MMP-3/TIMP-1 of coronary artery lesion group(CAL group) compared with Non-CAL group(NCAL group) were significantly higher(P0.05).TIMP-1 of NCAL group was significantly higher(P0.01);acute phase and convalescence phase MMP-3,TIMP-1 and the ratio of MMP-3/TIMP-1 were significantly higher(P0.01).NO of CAL group was significantly higher(P0.05).There was significantly positive correlation between NO and MMP-3 level.(r=0.898,P0.01),and there was significantly negative correlation between NO and TIMP-1 level in KD patients(r=-0.772,P0.01).Conclusion:MMP-3 of CAL group is significiantly higher than that of NCAL group.Therefore,the measurement of serum MMP-3 might be of important clinical value in prediction and early diagnosis of KD with coronary artery lesion.In acute stage serum MMP-3 and TIMP-1 levels and the ratio of MMP-3/TIMP-1 are higher in convalescent stage and control,suggesting that these data are important objective markers for diagnosis of KD in early stage.The overexpression of NO may play an important role in the development of acute stage of KD,suggesting that NO level in serum should be an important objective markers of coronary arterial lesion.
出处 《泸州医学院学报》 2011年第4期370-373,共4页 Journal of Luzhou Medical College
关键词 基质金属蛋白酶 基质金属蛋白酶抑制剂 一氧化氮 川崎病 冠脉损害 MMPs TIMPs Nitrie Oxide(NO) Kawasaki disease Coronary artery lesion(CAL)
  • 相关文献

参考文献9

  • 1Senzaki H,Masutani S,Kobayashi J,et al.Circulating matrix metalloproteinases and their inhibitors in patients with Kawasaki disease[J]. Circulation,2001 ; 104(8) :860.
  • 2Gavin PJ, Crawford SE, Shulman ST, et al.Systemic arterial expression of matrix metalloproteinases 2 and 9 in acute Kawasaki disease[J].Vasc Biol, 2003 ; 23 (4) : 576.
  • 3Yu X, Hirono KI,Ichida F, et al.Enhanced iNOS expre- ssion in leukocytes and circulating endothelial cells is associated with the progression of coronary artery lesions in acute Kawasaki disease[J].Pediatr Res,2004,55(4):688.
  • 4Ayuswa M , Sonobe T, Uemura S, et al. Revision of diagnostic guidelines for Kawasaki disease (the 5th revised edition) [J] .PediatrInt, 2005;47 ( 2 ) : 232.
  • 5吴瑞萍,胡亚美,江载芳,主编.实用儿科学[M].第6版,北京:人民卫生出版社,2002;687-694.
  • 6Senzaki H,Masutani S,Kobayashi J,et al.Circulating Matrix Metalloproteinases and their inhibitors in patients with Kawasaki Disease[J]. Circulation, 2001 ; 104 (8) :860.
  • 7张园海,何跃娥,项如莲,吴蓉洲,徐强,荣星,陈其.川崎病急性期血清对血管内皮细胞MMP-3和TNF—α表达的影响及丙种球蛋白的干预作用[J].浙江医学,2009,31(4):451-453. 被引量:5
  • 8Iizuka T,Oishi K, Sasaki M,et al.Nitric oxide and aneurysm formation in Kawasaki disease[J].Acta Paediatr. 1997 ;86(5) :470.
  • 9Ikemoto Y,Teraguchi M,Ono A,et al.Serial changes of plasma nitrate in the acute phase of Kawasaki disease [J]. Pediatr Int,2003 ; 45(4) : 421.

二级参考文献13

  • 1Senzaki H,The pathophysiology of coronary artery aneurysms in kawasaki disease:role of matrix metalloproteinases[J].Arch Dis Child,2006,91(10):847-851.
  • 2Senzaki H,Masutani S,Kobayashi J,et al.Circulating matrix metalloproteinases and their inhibitors in patients with Kawasakj disease[J].Circulation,2001,104(8):860-863.
  • 3Matsumoto H,Koga H,lida M,et al.Blockade of tumor necrosis factor-alpha-converting enzyme improves experimental small intestinal damage by decreasing matrix metalloproteinase-3 production in rats[J].Scand J Gastroenterol,2006,41(11):1320-1329.
  • 4Newburger J W,Takahashi M,Gerber M A,et al.Diagnosis.treatment,and long-term management of Kawasaki disease:a statement for health professionals from the Committee on Rheumatic Fever,Endocarditis,and Kawasaki Disease,Council on Cardiovascular Disease in the Young,American Heart Association[J].Pediatrics,2004,114(6):1708-1733.
  • 5Yoon S,Tromp G,Vongpunsawad S,et al.Genetic analysis of MMP3,MMP9,and PAI-1 in Finnish patients with abdominal aortic or intracranial aneurysms[J].Biochem Biophys Res Commun,1999,265(2):563-568.
  • 6Park J A,Shin K S,Kim Y W,et al.Polymorphism of matrix metalloproteinase-3 promoter gene as a risk factor for coronary artery lesions in kawasaki disease[J].J Korean Med Sci,2005,20(4):607-611.
  • 7Hui Yuen J S,Duong T T,Yeung R S,et al.TNF-alpha is necessary for induction of coronary artery inflammation and aneurysm formation in an animal model of Kawasaki disease[J].J Immunol,2006,76(10):6294-6301.
  • 8Kaneko K,Savage C O,Pottinger B E,et al.Antiendothelial cell antibodies can be cytotoxic to endothelial cells without cytokine re-stimulation and correlate with ELISA antibody measurement in kawasaki disease[J].Clin Exp Immunol,1994,98(2):264-269.
  • 9Sakata K,Kita M,Imanishi J,et al.Effect of Kawasaki disease on migration of human umbilical vein endothelial cells[J].Pediatr Res,1995,38(4):501-505.
  • 10Kazatchkine M D,Kaveri S V.Immunomodulation of autoimmune and infIamma tory diseases with intravenous immune globulin[J].N Engl J Med,2001,345(10):747-755.

共引文献4

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