Dietary Acacetin Reduces Airway Hyperresponsiveness and Eosinophil Infiltration by Modulating Eotaxin-1 and Th2 Cytokines in a Mouse Model of Asthma

Abstract EN

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.