Licochalcone A was isolated from Glycyrrhiza uralensis and previously reported to have antitumor and anti-inflammatory effects.
Licochalcone A has also been found to inhibit the levels of Th2-associated
cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. However, the molecular mechanism underlying airway
inflammation and how
licochalcone A regulates oxidative stress in asthmatic mice are elusive. In this study, we investigated whether
licochalcone A could attenuate inflammatory and oxidative responses in tracheal epithelial cells, and whether it could ameliorate oxidative stress and airway
inflammation in asthmatic mice. Inflammatory human tracheal epithelial (BEAS-2B) cells were treated with
licochalcone A to evaluate oxidative responses and inflammatory
cytokine levels. In addition, BALB/c mice were sensitized with
ovalbumin (OVA) and injected intraperitoneally with
licochalcone A (5 or 10 mg/kg).
Licochalcone A significantly inhibited
reactive oxygen species, eotaxin, and proinflammatory
cytokines in BEAS-2B cells.
Licochalcone A also decreased
intercellular adhesion molecule 1 levels in inflammatory BEAS-2B cells, blocking monocyte cell adherence. We also found that
licochalcone A significantly decreased oxidative responses, reduced
malondialdehyde levels, and increased
glutathione levels in the lungs of OVA-sensitized mice. Furthermore,
licochalcone A decreased
airway hyper-responsiveness, eosinophil infiltration, and Th2
cytokine production in the BALF. These findings suggest that
licochalcone A alleviates oxidative stress,
inflammation, and pathological changes by inhibiting Th2-associated
cytokines in asthmatic mice and human tracheal epithelial cells. Thus,
licochalcone A demonstrated therapeutic potential for improving
asthma.