论文部分内容阅读
目的研究尾加压素Ⅱ(UⅡ)及其受体拮抗剂Urantide(UR)对培养的大鼠肺动脉平滑肌细胞(PASMCs)增殖及Ⅰ、Ⅲ型胶原合成的影响。方法以组织贴块法培养的大鼠PASMCs为研究对象,采用BrdU掺入实验观察不同浓度UⅡ(1×10-10～1×10-7mol/L)及Urantide对PASMCs增殖的影响;采用Western blotting及Real-timePCR法,分别在蛋白和基因水平检测不同浓度UⅡ及Urantide对Ⅰ、Ⅲ型胶原合成的影响。结果 UⅡ(1×10-9～1×10-7mol/L)浓度依赖性地促进PASMCs增殖(P<0.05,P<0.001,P<0.001),增加PASMCs中Ⅰ、Ⅲ型胶原基因及蛋白表达(P<0.01,P<0.001),而1×10-10mol/L UⅡ对PASMCs增殖及Ⅰ、Ⅲ胶原基因和蛋白表达无明显作用(P>0.05);UⅡ受体拮抗剂Urantide可拮抗UⅡ的上述作用(P<0.01)。结论 UⅡ通过与大鼠PASMCs的UⅡ受体UT结合而发生一系列诱导作用,最终引起PASMCs增殖及Ⅰ、Ⅲ型胶原合成增加,Urantide通过竞争性结合UT而阻断UⅡ与UT的结合,使UⅡ无法发挥诱导作用。
Objective To investigate the effects of urotensin Ⅱ (UⅡ) and its receptor antagonist Urantide (UR) on the proliferation of rat pulmonary artery smooth muscle cells (PASMCs) and the synthesis of type Ⅰ and type Ⅲ collagen. Methods PASMCs cultured in tissue-patch method were used as experimental subjects. BrdU incorporation assay was used to observe the effects of different concentrations of UⅡ (1 × 10-10 ~ 1 × 10-7 mol / L) and Urantide on the proliferation of PASMCs. Western blotting And Real-time PCR method were used to detect the effects of different concentrations of UⅡ and Urantide on the type I and type Ⅲ collagen synthesis at the protein and gene level respectively. Results UⅡ (1 × 10-9 ~ 1 × 10-7 mol / L) promoted the proliferation of PASMCs in a concentration-dependent manner (P <0.05, P <0.001, P <0.001) and increased the expression of collagen type Ⅰ and type Ⅲ (P <0.01, P <0.001). However, U × 10-10 mol / L UⅡ had no effect on the proliferation of PASMCs and the gene and protein expression of collagen Ⅰ and Ⅲ (P> 0.05). Urantide, a UⅡreceptor antagonist, The above effect (P <0.01). CONCLUSION: UⅡ exerts a series of induction effects through the binding of UⅡ receptor UT to rat PASMCs, which eventually leads to the proliferation of PASMCs and the increase of type Ⅰ and Ⅲ collagen synthesis. Urantide blocks the binding of UⅡ and UT through competitive binding of UT, Can not play an inductive role.