期刊文献+

高肺血流对大鼠肺动脉胶原水平及代谢的影响

Impact of High Pulmonary Blood Flow on Content and Metabolism of Collagen in Rats
下载PDF
导出
摘要 目的探讨高肺血流对大鼠肺动脉胶原水平及代谢的影响。方法雄性SD大鼠32只,随机均分为分流组和对照组,对分流组大鼠行腹主动脉-下腔静脉穿刺术建立高肺血流动物模型。分别在分流术后4、11周2个时间点处死大鼠留取肺组织标本(每组n=8)。制作肺组织石蜡切片,以免疫组织化学方法检测肺动脉胶原Ⅰ、胶原Ⅲ、金属基质蛋白酶-13(MMP-13)及其抑制物-1(TIMP-1)表达的变化。结果分流后4、11周,与对照组比较,大鼠肺动脉胶原Ⅰ、胶原Ⅲ、MMP-13及TIMP-1表达明显增强(P<0.05)。结论高肺血流上调大鼠肺动脉胶原Ⅰ和胶原Ⅲ表达,该作用可能参与介导高肺血流致肺血管结构重建的机制。 Objective To explore impact of high pulmonary blood flow on the content and metaholism of collagen in rats. Methods Thirty - two male SD rats were randomly divided into shunt group and control group. Rats in shunt group were subjected to an abdominal aorta - inferior vena eava shunt to create an animal model of high pulmonary blood flow. In control group, rats experienced the same experimental processes except the shunting procedure. After 4 and 11 weeks of experiment, these changes of pulmonaryartery collagen Ⅰ, col- lagen Ⅲ,matrix metalloproteinase(MMP- 13)and tissue inhibitor of metalloproteinase(TIMP- 1) protein expression of rat Were investigated by immunohistochemistry. Results After 4 weeks and 11 weeks of shunt,the collagen Ⅰ,collagen Ⅲ ,MMP- 13 and TIMP- 1 of pulmonary artery in rats of shunt group increased significantly compared with those of control group, respectively(all P 〈0,05). Conclusions High pulmonary blood flow up - regulates the pulmonary artery collagen Ⅰ and collagen Ⅲ protein expression in rats,which may be involved in the mechanism of pulmonary vascular structural remodeling induced by high pulmonary blood flow.
出处 《实用儿科临床杂志》 CAS CSCD 北大核心 2006年第23期1635-1636,共2页 Journal of Applied Clinical Pediatrics
基金 国家杰出青年科学基金项目资助(30425010) 国家重点基础研究发展规划(2006CB503807) 北京市自然科学基金项目资助(7052043)
关键词 高肺血流 胶原 大鼠 high pulmonary blood flow collagen rat
  • 引文网络
  • 相关文献

参考文献4

二级参考文献50

  • 1石瑛,杜军保,张春雨,唐朝枢.硫化氢对低氧大鼠肺动脉金属蛋白酶组织抑制因子-1基因表达的影响[J].实用儿科临床杂志,2004,19(11):928-930. 被引量:6
  • 2孙仁宇,严仪昭,陈祥银,云登卓玛,李红兵.血管胶原代谢改变及其在大鼠低氧性肺动脉高压形成中的作用[J].基础医学与临床,1993,13(5):45-49. 被引量:7
  • 3薛全福,谢剑鸣.常压缺氧性大鼠肺动脉高压模型的建立[J].中华结核和呼吸杂志,1989,12(6):350-352. 被引量:157
  • 4Spinale FG, Coker ML, Bond BR, et al. Myocardial matrix degradation and metalloproteinase activation in the failing heart : a potential therapeutic target. Cardilvasc Res, 2000, 46:225-238. 被引量:1
  • 5Saharinen J, Hyytiainen M, Taipale J, et al. Latent transforming growth factor-beta binding proteins ( LTBPs ) structural extracellular nmtrix proteins for targeting TGF-beta action. Cytokine Growth Factor Rev, 1999, 10 : 99-117. 被引量:1
  • 6Peterson JT, Li H, Dillon L, et al. Evolution of matrix metalloproteinase and tissue inhibitor expression during heart failure progression int infracted rat. Cardiovasc Res, 2000, 46:307-315. 被引量:1
  • 7Nagahiro N, Kazuhiro Y, Yasushi S, et al. Differential activation of matrix metalloproteinases in heart failure with and without ventricular dilatation. Cardiovasc Res, 2003, 57:766-774. 被引量:1
  • 8Ducharme A , Frantz S, Aikawa M, et al. Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction. J Clin Invest, 2000, 106:55-62. 被引量:1
  • 9Heymans S, Luttun A, Nuyens D, et al. Inhibition of plasminogen activators or matrix metallproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure . Nat Med, 1999, 5:1135-1142. 被引量:1
  • 10Borg TK, Burgess ML. Holding it all together: organization and function(s) of the extracellular matrix of the heart. Heart Failure,1993,8 : 230-238. 被引量:1

共引文献62

;
使用帮助 返回顶部