中文摘要：

目的观察缓激肽对转化生长因子-β1（TGF-β1）诱导的肺动脉平滑肌细胞（PASMCs）迁移的影响及其可能机制。方法原代培养PASMCs，应用Transwell小室检测缓激肽对PASMCs跨膜迁移能力的影响，同时应用划痕修复实验检测缓激肽对PASMCs横向迁移能力的影响。结果TGF-β1显著增加了跨膜迁移的PASMCs数目（P〈O．05），缓激肽显著减少了PASMCs的跨膜迁移（P〈O．05），而B2受体抑制剂（HOE-140）对缓激肽抑制TGF-β1诱导的PASMCs的跨膜迁移作用无显著改变（P〉0．05）。缓激肽显著降低PASMCs的划痕愈合指数（P〈0．05），而HOE-140对缓激肽抑制TGF-β1诱导的PASMCs的横向迁移能力无显著改变（P〉0．05）。结论缓激肽可以抑制TGF-β1诱导的PASMCs跨膜和横向迁移能力，而这一效应可能不通过缓激肽B2受体介导。

英文摘要：

Objective To study the effects of bradykinin （BK） on pulmonary artery smooth muscle cells （PASMCs） migration induced by transforming growth factor-β1 （TGF-β1） and their possible mechanisms. Methods The transmembrane migration of BK on primary PASMCs with TGF-β1 treatment was examined by transwell assay, and the lateral migration of BK on primary PASMCs with TGF-β1 was determined by healing of surface scratch assay. Results TGF-β1 significantly increased the number of PASMCs migrating across the membrane （P 〈 O. 05 ）. BK significantly reduced TGF-β1 induced PASMCs transmembrane migration （P〈0.05）, which was not prevented by the B2 receptor （B2R） inhibitor HOE-140 （P〉0.05）. Furthermore, BK significantly reduced TGF-β1 -induced PASMCs lateral migration （P〈0.05） , while the effect was not blocked by the B2R inhibitor HOE-140 （P 〉 0. 05 ）. Conclusion BK can significantly inhibit TGF-β1-induced PASMCs transmembrane and lateral migration. However the inhibitory effects of migration may not be mediated by bradykinin B2 receptor.