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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 mechanism of airway epithelial cells on fibroblast growth. Methods An indirect airway remodeling cell model was established. Tyrosine kinase inhibitors (TKIs) Tyrphostin AG1478 and gold metastasis were used as intervention factors. 3H-DdR incorporation was used to observe the effects of different concentrations of tracheal epithelial cells The effect of supernatant on the growth of fibroblasts was examined by ELISA. The changes of epidermal growth factor (EGF) and transforming growth factor β1 (TGFβ1) in supernatants were detected by ELISA. Results The proliferation of fibroblasts was stimulated by 50% supernatant of epithelial cells of injured group. The pretreatment of TKIs with 50μmol / L for 30min could reduce the stimulation of fibroblasts. TGFβ1 in supernatant of injured group was significantly decreased, L of TKIs pretreatment can make the supernatant TGFβ1 was significantly increased; EGF was not detected in each group. Conclusion Epithelial injury can indirectly lead to the proliferation of fibroblasts. Pretreatment with certain concentration of TKIs for 30 min after epithelial injury can inhibit this proliferation effect to a certain extent. TKIs may play a preventive role in airway remodeling.