
The study evaluated the effects of fisetin on airway remodeling and the phenotypic transition of airway smooth muscle cells (ASMCs) in ovalbumin (OVA)-induced asthma. Network pharmacology identified the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway as a target. In vivo, fisetin administration reduced airway inflammation and remodeling in asthmatic mice, evidenced by decreased inflammatory cells, Th2 cytokines, collagen accumulation, and ASMC thickening. In vitro, fisetin downregulated synthetic and contractile phenotypic proteins and inhibited ASMC migration, likely via the PI3K/AKT pathway. These results suggest fisetin may be a promising candidate for treating airway remodeling in asthma.
Like
Save
Share