Abstract
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.
Highlights
Asthma is an important health problem, with continually increasing prevalence and mortality in developing and developed countries [1,2]
airway hyper-responsiveness (AHR) was assessed on day 28, and mice were sacrificed to OVA group, asthmatic mice treated with licochalcone A had significantly reduced numbers of evaluate asthma pathology, oxidative pressure, immune regulation, and inflammatory response on eosinophils and total cells (Figure 1E)
Airway resistance as detected by the forced intubation technique demonstrated that 10 mg/kg licochalcone A significantly attenuated airway resistance and increased dynamic lung compliance compared to OVA (Figure 1B,C)
Summary
Asthma is an important health problem, with continually increasing prevalence and mortality in developing and developed countries [1,2]. Several studies have demonstrated that allergic asthma is an immune imbalance in which overactivation of Th2 cells increases the secretion of IL-4, IL-5, and IL-13 cytokines [5] These Th2-associated cytokines would induce eosinophil infiltration, inducing inflammation and the allergy response, stimulate goblet cell hyperplasia for excessive mucus secretion, and exacerbate IgE production to induce mast cell activation and cause a severe allergic reaction [6]. Inflammatory respiratory epithelial cells release high levels of chemokines for attracting eosinophilic infiltration to aggravate airway inflammation [1,9]. These epithelial cells release excessive ROS, inducing airway remodeling, abnormal smooth muscle thickness, and AHR [10]
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