We have explored the role of hyperin remodeling of airway smooth muscle cells during asthma. To this end, airway smooth muscle cells were isolated from tracheae and bronchi of mice, treated with transforming growth factor-β1 and increasing concentrations of hyperin followed by analysis of cell viability, proliferation, and migration. The levels of extracellular matrix formation were evaluated by analysis of fibronectin and type I collagen. Western blot analysis was used to assess the function of the downstream pathway of nuclear factor-kappa B. Transforming growth factor-β1 treatment led to a dose-dependent increase in type I collagen and fibronectin that was reversed by hyperin. Transforming growth factor-β1 promoted activation of nuclear factor-kappa B pathway with reduced IκBα and enhanced phospho (p)-p65 and p-IκBα. However, hyperin treatment upregulated IκBα and downregulated p-p65/p-IκBα to inactivate NF-κB pathway. In conclusion, hyperin ameliorates proliferation, migration, and extracellular matrix formation in airway smooth muscle cells by inhibiting transforming growth factor-β1-induced nuclear factor-kappa B activation suggesting potential prevention of airway remodeling during asthma.
Transforming Growth Factor-β and Nuclear Factor E2–related Factor 2 Regulate Antioxidant Responses in Airway Smooth Muscle Cells
