Asthma is recognized as a chronic respiratory illness
characterized
by airway inflammation and airway hyperresponsiveness. Wogonoside,
a flavonoid glycoside, is reported to significantly alleviate the
inflammation response and oxidative stress. Herein, this study aimed
to investigate the therapeutic effect and underlying mechanism of
wogonoside on airway inflammation and mucus hypersecretion in a murine
asthma model and in human bronchial epithelial cells (16HBE). BALB/c
mice were sensitized and challenged with ovalbumin (OVA). Pulmonary
function and the number of cells in the bronchoalveolar lavage fluid
(BALF) were examined. Pathological changes in lung tissue in each
group were evaluated via hematoxylin and eosin and periodic acid–Schiff
staining, and changes in levels of cytokines in BALF and of immunoglobulin
E in serum were determined via an enzyme-linked immunosorbent assay.
The expression of relevant genes in lung tissue was analyzed via real-time
PCR. Western blotting and immunofluorescence were employed to detect
the expression of relevant proteins in lung tissue and 16HBE cells.
Treatment with 10 and 20 mg/kg wogonoside significantly attenuated
the OVA-induced increase of inflammatory cell infiltration, mucus
secretion, and goblet cell percentage and improved pulmonary function.
Wogonoside treatment reduced the level of T-helper 2 cytokines including
interleukin (IL)-4, IL-5, and IL-13 in BALF and of IgE in serum and
decreased the mRNA levels of cytokines (IL-4, IL-5, IL-6, IL-13, and
IL-1β and tumor necrosis factor-α), chemokines (CCL-2,
CCL-11, and CCL-24), and mucoproteins (MUC5AC, MUC5B, and GOB5) in
lung tissues. The expression of MUC5AC and the phosphorylation of
STAT6 and NF-κB p65 in lung tissues and 16HBE cells were significantly
downregulated after wogonoside treatment. Thus, wogonoside treatment
may effectively decrease airway inflammation, airway remodeling, and
mucus hypersecretion via blocking NF-κB/STAT6 activation.