缓激肽对TGF-β_1诱导的猪肺动脉平滑肌细胞增殖的影响  

Effects of bradykinin on proliferation of porcine pulmonary artery smooth muscle cells induced by TGF-β_1

作　　者：冯文静[1] 徐西振[2] 赵刚[3] 赵俊杰[1] 董若兰[1] 凃玲[1] 姚济华[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院老年医学科,湖北武汉430030 [2]华中科技大学同济医学院附属同济医院心内科,湖北武汉430030 [3]山东大学附属省立医院心内科,山东济南250021

出　　处：《中国病理生理杂志》2013年第10期1736-1740,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.81170111;No.81100085;No.30971247)

摘　　要：目的:研究缓激肽(BK)对转化生长因子β1(TGF-β1)诱导的肺动脉平滑肌细胞(PASMCs)增殖的影响及其可能机制。方法:原代培养猪PASMCs,采用CCK-8法测定BK对TGF-β1诱导的PASMCs增殖能力的影响,同时应用Western blotting检测PASMCs PI3K、p-Akt和p-ERK1/2表达的变化。结果:TGF-β1呈剂量依赖性促进PASMCs增殖(P<0.05),BK显著抑制了TGF-β1诱导的PASMCs增殖(P<0.05),而BK 2型受体(B2R)抑制剂HOE-140可以显著抑制BK的效应(P<0.05);Western blotting结果显示,BK抑制TGF-β1诱导的PASMCs增殖主要是通过阻断PI3K/Akt和ERK1/2信号通路活化而实现。结论:BK显著抑制TGF-β1诱导的PASMCs增殖,此作用可能与其抑制PI3K/Akt和ERK1/2信号通路活化有关。AIM：To investigate the effects of bradykinin （BK） on the proliferation of pulmonary artery smooth muscle cells （PASMCs） induced by transforming growth factor beta 1 （TGF-β1） and its possible mechanisms. METHODS：Primary porcine PASMCs were isolated, cultured and identified, and the cells at passages 2~6 were used in this study. The viability of PASMCs was determined by Cell Counting Kit-8 assay. The protein expression of phosphatidylinositol 3-kinase （PI3K）, phosphorylated Akt （p-Akt） and phosphorylated extracellular signal-regulated kinase 1/2 （p-ERK1/2） was detected by Western blotting. RESULTS：TGF-β1 promoted the proliferation of PASMCs in a dose-dependent manner （P〈005）. BK significantly inhibited the proliferation of PASMCs induced by TGF-β1 （P〈005）, and attenuated the elevated expression of PI3K, p-Akt and p-ERK1/2 proteins （P〈005）. HOE-140, a BK type 2 receptor （B2R） inhibitor, reversed the effects of BK （P〈005）. CONCLUSION：BK inhibits TGF-β1-induced proliferation of PASMCs, which may be associated with inactivation of PI3K/Akt and ERK1/2 signaling pathways.

关 键 词：缓激肽 肺动脉平滑肌细胞 转化生长因子Β1 细胞增殖 

分 类 号：R363[医药卫生—病理学]