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野百合碱诱导大鼠肺高压时韧粘素mRNA表达水平的动态变化
引用本文:沈捷,周爱卿,秦玉明,梁瑛,李奋. 野百合碱诱导大鼠肺高压时韧粘素mRNA表达水平的动态变化[J]. 中国当代儿科杂志, 2001, 3(5): 519-521
作者姓名:沈捷  周爱卿  秦玉明  梁瑛  李奋
作者单位:沈捷,周爱卿,秦玉明,梁瑛,李奋
基金项目:上海市高等学校科学技术发展基金资助项目 ( 98B2 0 )
摘    要:目的:观察野百合碱(MCT)所致肺高压大鼠肺组织和肺动脉中韧粘素(TN)mRNA的动态表达水平,探讨其与肺高压肺血管重建的关系。方法:SD大鼠随机分为MCT组和正常对照组(CON),采用野百合碱皮下注射法诱导建立大鼠肺高压模型,并通过快速竞争性RT PCR技术检测不同时间点(给药后第7,14,21,28天)大鼠肺组织和肺动脉中TNmRNA的表达水平。结果:TN mRNA水平在给药后第7天即有上调,CON组肺组织TNmRNA为0.29±0.04,MCT组为0.56±0.08,两组间差异有显著性(P<0.01);CON组肺动脉TN mRNA 为0.30±0.04,MCT组为0.57±0.05,两组间差异有显著性(P<0.05)。TN mRNA水平上调早于肺动脉压的升高,随压力上升和时间延长TN mRNA继续增高。结论:TN参与了肺高压肺血管重建过程,在肺高压发病中可能具有重要作用。

关 键 词:韧粘素  细胞外基质  肺动脉高压  血管重建  大鼠  
文章编号:1008-8830(2001)05-0519-03
修稿时间:2001-01-08

Levels of Tenascin mRNA in Monocrataline Induced Pulmonary Hypertension in Rats
SHEN Jie,ZHOU Ai-Qing,QIN Yu-Ming,LIANG Ying,LI Fen. Levels of Tenascin mRNA in Monocrataline Induced Pulmonary Hypertension in Rats[J]. Chinese journal of contemporary pediatrics, 2001, 3(5): 519-521
Authors:SHEN Jie  ZHOU Ai-Qing  QIN Yu-Ming  LIANG Ying  LI Fen
Affiliation:SHEN Jie, ZHOU Ai-Qing, QIN Yu-Ming, LIANG Ying, LI Fen
Abstract:Objective To study the levels of Tenascin (TN) mRNA in pulmonary vascular remodeling associated with pulmonary hypertension(PH) induced by monocrataline (MCT). Methods SD rats were randomly assigned into the control (CON) group and MCT group. The model of PH was created by injecting hypodermatic MCT. Rapid competitive RT PCR was used to examine the levels of TN mRNA in central pulmonary arteries (PAs) and lungs at different times after MCT or NS injections. Results Increased expression of TN mRNA was detected 7 days after the injection of MCT. The expression of TN mRNA in lungs of the MCT group ( 0.56 ± 0.08 ) was higher than that of the CON group ( 0.29 ± 0.04 ),P< 0.01 . TN mRNA in PAs of the MCT group ( 0.57 ± 0.05 ) was higher than that of the CON group ( 0.30 ± 0.04 ),P< 0.05 . The increase of the level of TN mRNA preceded the elevation of pulmonary pressure (14 days) and continued to increase with the rising of pulmonary pressure. Conclusions TN might be involved in the pathogenesis of pulmonary vascular remodeling with PH.
Keywords:Tenascin  Extracelluar matrix  Pulmonary hypertension  Vascular remodeling  Rat
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