Tectorigenin regulates migration, invasion, and apoptosis in dexamethasone‐induced human airway epithelial cells through up‐regulating miR‐222‐3p

摘要: Glucocorticoids (GCs) can effectively control airway inflammation, but also cause epithelial injury. Tectorigenin, a type of isoflavone isolated from various medicinal plants, has hypolipidemic activity, hepatoprotective, and antioxidant effects. We aimed to investigate whether Tectorigenin repair GCs-induced Airway cell line (9HTE cells) were treated with dexamethasone (Dex), or further transfected, then viability, migration, invasion examined by Cell Counting Kit (CCK-8), wound healing, Transwell assays. The expressions potential miRNAs related the effect detected quantitative polymerase chain reaction (qPCR). Expressions poptosis-related proteins Bcl-2-associated protein-X (Bax), B-cell lymphoma-2 (Bcl-2), Cleaved Caspase-3, Mitorgen-activated protein kinase (MAPK) signaling pathway serine/threonine (Raf1), extracellular signal-regulated 1/2 (MEK1/2), (ERK1/2) Western blot. Dex inhibited migration promoting Bax Caspase-3 (p <.001) inhibiting Bcl-2 miR-222-3p <.001). Then, 10 μmol/L itself did not affect viability could inhibit on invasion. up-regulated miR-222-3p, Bcl-2, p-Raf1, p-MEK1/2, p-ERK1/2 <.01), down-regulated <.05) in Dex-induced cells. MiR-222-3p inhibitor reversed antagonistic Dex. study demonstrates that inhibits apoptosis 9HTE cells up-regulating expression which involves MAPK pathway.