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Procaterol Inhibits Lung Fibroblast Migration

机译:丙卡特罗抑制肺成纤维细胞迁移

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Fibroblasts are important cells that are involved in modulation of fibrosis after injuries. In some uncontrollable inflammatory processes, excess fibroblasts migrate around the small airway. The pathogenesis of chronic obstructive pulmonary disease is related to fibrosis around the small airways. The aim of the current study was to investigate the effect of procaterol, a second-generation beta (2)-agonist, on migration of human fetal lung fibroblasts (HFL-1) induced by human plasma fibronectin (HFn). Using the blindwell chamber technique, 10−8 M procaterol inhibited migration of HFL-1 (control, 100%; 10−8 M, 73.2 ± 4.9%; n = 6, p < 0.05). The inhibitory effect of procaterol was concentration-dependent. Although a beta 2-receptor inhibitor, ICI 181551, blocked the inhibitory effect of procaterol, a beta 1-receptor inhibitor, atenolol, did not. Because a cyclic AMP-dependent protein kinase (PKA) inhibitor, KT5720, blocked the effect of procaterol, the cyclic AMP–PKA pathway may be involved in the migration inhibitory process. Procaterol, which is prescribed mainly for treatment of bronchial asthma, might be a useful drug for inhibiting lung fibrosis following injuries to the lung.
机译:成纤维细胞是重要的细胞,参与损伤后纤维化的调节。在某些无法控制的炎症过程中,过量的成纤维细胞在小气道周围迁移。慢性阻塞性肺疾病的发病机制与小气道周围的纤维化有关。本研究的目的是研究第二代β(2)激动剂丙卡特罗对人血浆纤连蛋白(HFn)诱导的人胎肺成纤维细胞(HFL-1)迁移的影响。使用盲孔室技术,10 −8 M儿茶酚抑制HFL-1迁移(对照,100%; 10 -8 M,73.2±4.9%; n = 6 ,p <0.05)。丙卡特罗的抑制作用是浓度依赖性的。尽管β2受体抑制剂ICI 181551阻断了丙卡特罗的抑制作用,但β1受体抑制剂阿替洛尔却没有。由于环状AMP依赖性蛋白激酶(PKA)抑制剂KT5720阻断了丙卡特罗的作用,因此环状AMP–PKA途径可能参与了迁移抑制过程。主要用于治疗支气管哮喘的丙卡特罗可能是抑制肺损伤后肺纤维化的有用药物。

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