Fucoxanthin is isolated from brown algae and was previously reported to have multiple pharmacological effects, including anti-
tumor and anti-
obesity effects in mice.
Fucoxanthin also decreases the levels of inflammatory
cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. The purpose of the present study was to investigate the effects of
fucoxanthin on the oxidative and inflammatory responses in inflammatory human tracheal epithelial BEAS-2B cells and attenuated
airway hyperresponsiveness (AHR), airway
inflammation, and oxidative stress in asthmatic mice.
Fucoxanthin significantly decreased monocyte cell adherence to BEAS-2B cells. In addition,
fucoxanthin inhibited the production of pro-inflammatory
cytokines, eotaxin, and
reactive oxygen species in BEAS-2B cells.
Ovalbumin (OVA)-sensitized mice were treated by
intraperitoneal injections of
fucoxanthin (10 mg/kg or 30 mg/kg), which significantly alleviated AHR, goblet cell
hyperplasia and eosinophil infiltration in the lungs, and decreased Th2
cytokine production in the BALF. Furthermore,
fucoxanthin significantly increased
glutathione and
superoxide dismutase levels and reduced
malondialdehyde (MDA) levels in the lungs of asthmatic mice. These data demonstrate that
fucoxanthin attenuates
inflammation and oxidative stress in inflammatory tracheal epithelial cells and improves the pathological changes related to
asthma in mice. Thus,
fucoxanthin has therapeutic potential for improving
asthma.