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目的研究结缔组织生长因子(CTGF)在高肺血流性肺动脉高压大鼠模型中的表达及法舒地尔对其的调控作用。方法将75只W istar大鼠分为对照组、2个分流组和2个分流+法舒地尔干预组,每组15只。对照组于第4周测量右心室平均收缩压(RVSP)、2个分流组和2个分流+法舒地尔干预组分别于第2周和第4周测量RVSP。采用W estern b lot法和免疫组化检测各组肺动脉中CTGF、转化生长因子β1(TGFβ-1)的含量以及Rho激酶的活性。结果分流组大鼠第2周及第4周肺动脉明显增厚(P<0.01)、重塑,RVSP增加(P<0.01),CTGF及TGFβ-1表达增加(P<0.01),且Rho激酶活性增强(P<0.01)。应用法舒地尔干预后,肺动脉Rho激酶活性明显降低(P<0.01),且CTGF和TGFβ-1在肺动脉中的表达较分流组明显降低(P<0.01)、肺血管重塑较分流组显著减轻(P<0.01)。结论CTGF,TGFβ-1参与了高肺血流性肺动脉高压的发病过程,且Rho激酶信号转导通路对肺血管的重塑及CTGF,TGFβ-1的表达有着重要的调控作用。
Objective To study the expression of connective tissue growth factor (CTGF) in rat model of pulmonary hypertension induced by high pulmonary blood flow and the effect of fasudil on it. Methods Seventy-five Wistar rats were divided into control group, 2 shunt groups and 2 shunt + fasudil intervention groups, with 15 rats in each group. RVSP was measured in the control group at 4 weeks, RVSP was measured at 2 weeks and 4 weeks in the 2 shunt groups and 2 shunt + fasudil intervention groups, respectively. The levels of CTGF, transforming growth factor β1 (TGFβ-1) and Rho kinase in the pulmonary arteries were detected by Western blot and immunohistochemistry. Results Pulmonary artery was significantly thicker (P <0.01), remodeling, RVSP increased (P <0.01), the expression of CTGF and TGFβ-1 in the shunt group was significantly increased at the second week and the fourth week (P <0.01) Enhanced (P <0.01). Pulmonary artery Rho kinase activity was significantly decreased (P <0.01) after application of fasudil intervention, and the expression of CTGF and TGFβ-1 in pulmonary artery was significantly lower than that in shunt group (P <0.01). Pulmonary vascular remodeling was more significant than shunt group Reduce (P <0.01). Conclusion CTGF and TGFβ-1 are involved in the pathogenesis of pulmonary hypertension with high pulmonary blood flow. Rho kinase signaling pathway plays an important role in the regulation of pulmonary vascular remodeling and the expression of CTGF and TGFβ-1.