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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 7,14,2 1,2 8天 )大鼠肺组织和肺动脉中TNmRNA的表达水平。结果 TNmRNA水平在给药后第 7天即有上调 ,CON组肺组织TNmRNA为 0 .2 9± 0 .0 4,MCT组为 0 .5 6± 0 .0 8,两组间差异有显著性 (P <0 .0 1) ;CON组肺动脉TNmRNA为0 .30± 0 .0 4,MCT组为 0 .5 7± 0 .0 5 ,两组间差异有显著性 (P <0 .0 5 )。TNmRNA水平上调早于肺动脉压的升高 ,随压力上升和时间延长TNmRNA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。
Objective To observe the dynamic expression of fibronectin (TN) mRNA in lung tissue and pulmonary artery of monocrotaline (MCT) -induced pulmonary hypertension in rats and its relationship with pulmonary vascular remodeling. Methods SD rats were randomly divided into MCT group and normal control group (CON). Hypothalamic model was established by subcutaneous injection of monocrotaline, and rapid competitive RT-PCR was used to detect different time points (7 , 14, 2, 12 days). The levels of TNmRNA in lung tissue and pulmonary artery of rats. Results The level of TNmRNA was up-regulated on the 7th day after administration. The TNmRNA in CON group was 0.29 ± 0. 04 in CON group and 0.56 ± 0.08 in MCT group, with significant difference between the two groups (P <0.01). The pulmonary artery TN mRNA in CON group was 0.30 ± 0. 04, MCT group was 0. 57 ± 0. 05, there was significant difference between the two groups (P <0.05 ). The level of TNmRNA was up-regulated earlier than the increase of pulmonary arterial pressure, TNmRNA increased with the increase of pressure and time. Conclusions TN is involved in the pulmonary vascular remodeling and may play an important role in the pathogenesis of pulmonary hypertension.