摘要
目的探讨气道上皮细胞对成纤维细胞生长的调节机制。方法应用一种间接的气道重构的细胞模型,以酪氨酸激酶抑制剂(TKIs)TyrphostinAG1478及金转停为干预因素,用3HTdR掺入法观察大鼠气管上皮细胞不同损伤状态下培养上清液对成纤维细胞生长的影响,用ELISA方法检测上清液中表皮生长因子(EGF)及转化生长因子β1(TGFβ1)的变化。结果损伤组上皮的50%培养上清液刺激成纤维细胞的增殖,上皮损伤后50μmol/L的TKIs预处理30min可减弱其刺激作用;损伤组上皮细胞的上清液中TGFβ1明显降低,50μmol/L的TKIs预处理后可使上清液中TGFβ1明显增高;各组中均未检测出EGF。结论上皮损伤可间接导致成纤维细胞增殖,上皮损伤后一定浓度的TKIs预处理30min则可一定程度地抑制此种增殖效应,TKIs对气道重构的发生可能有一定预防作用。
Objective To investigate the regulatory effeets of airway epithelial cells and its mechanism on the growth of fibroblasts. Methods An imlirect ceellular model of airway remodeling was established and tyrosine kinase inhibitors（TKIs）tyrphostin AG1478 and Geinstein were used as interventional agents. The impact of conditioned medium（ CM）of rat trachea epithelial cells on different damaged conditions on fihroblasts proliferation assayed by 3H-thymidine （^3H-TdR）uptake wan ohserved. Meanwhile, ELISA was performed to detect EGF and TGF-β1 in CMs.Results 50% CM of damaged epithelial cells stimulated proliferation of fibroblasts and TKIs can reduce this efteet. Concentrations of TGF-β1 in CM from damaged epithelium were decreased and 50μmol/L of TKIs can increase concentrations of TGF-β1 in these CMs, EGF was not detected in CMs at any concentrations. Conclusions Epithelium injurt resuhs in a growth of fibroblasts indirectly. TKIs may inhihit this progress and may have a proteetive effect on airway remodeling.
出处
《中国呼吸与危重监护杂志》
CAS
2005年第5期385-388,共4页
Chinese Journal of Respiratory and Critical Care Medicine
基金
四川省科技厅应用基础项目(02SY029157)
