A previous study found that eosinophil infiltration and Th2 cell recruitment are important causes of chronic
lung inflammation in
asthma. The plant
flavonoid acacetin is known to have an anti-inflammatory effect in vitro. This study aims to investigate the anti-inflammatory effect of orally administered
acacetin in
ovalbumin- (OVA-) sensitized asthmatic mice and its underlying molecular mechanism. BALB/c mice were sensitized by intraperitoneal OVA injection. OVA-sensitized mice were fed
acacetin from days 21 to 27.
Acacetin treatment attenuated
airway hyperresponsiveness and reduced eosinophil infiltration and goblet cell
hyperplasia in lung tissue. Additionally, eotaxin-1- and Th2-associated
cytokines were inhibited in bronchoalveolar lavage fluid and suppressed the level of OVA-
IgE in serum. Human bronchial epithelial (BEAS-2B) cells were used to examine the effect of
acacetin on proinflammatory
cytokines,
chemokines, and
cell adhesion molecule production in vitro. At the molecular level,
acacetin significantly reduced
IL-6,
IL-8,
intercellular adhesion molecule-1, and
eotaxin-1 in activated BEAS-2B cells.
Acacetin also significantly suppressed the ability of eosinophils to adhere to inflammatory BEAS-2B cells. These results suggest that dietary
acacetin may improve
asthma symptoms in OVA-sensitized mice.