Abstract
Allergic asthma is a lifelong airway condition that affects people of all ages. In recent decades, asthma prevalence continues to increase globally, with an estimated number of 250,000 annual deaths attributed to the disease. Although inhaled corticosteroids and β-adrenergic receptor agonists are the primary therapeutic avenues that effectively reduce asthma symptoms, profound side effects may occur in patients with long-term treatments. Therefore, development of new therapeutic strategies is needed as alternative or supplement to current asthma treatments. Sesamin is a natural polyphenolic compound with strong anti-oxidative effects. Several studies have reported that sesamin is effective in preventing hypertension, thrombotic tendency, and neuroinflammation. However, it is still unknown whether sesamin can reduce asthma-induced allergic inflammation and airway hyperresponsiveness (AHR). Our study has revealed that sesamin exhibited significant anti-inflammatory effects in ovalbumin (OVA)-induced murine asthma model. We found that treatments with sesamin after OVA sensitization and challenge significantly decreased expression levels of interleukin-4 (IL-4), IL-5, IL-13, and serum IgE. The numbers of total inflammatory cells and eosinophils in BALF were also reduced in the sesamin-treated animals. Histological results demonstrated that sesamin attenuated OVA-induced eosinophil infiltration, airway goblet cell hyperplasia, mucus occlusion, and MUC5AC expression in the lung tissue. Mice administered with sesamin showed limited increases in AHR compared with mice receiving vehicle after OVA challenge. OVA increased phosphorylation levels of IκB-α and nuclear expression levels of NF-κB, both of which were reversed by sesamin treatments. These data indicate that sesamin is effective in treating allergic asthma responses induced by OVA in mice.
Highlights
Allergic asthma is a chronic airway inflammatory disease that affects over 300 million people worldwide [1]
Our results revealed that sesamin decreased OVA-induced secretion of IgE and cytokines, prevented eosinophil infiltration, and attenuated mucus oversecretion, likely by a mechanism of upregulating IkB-a and inhibiting nuclear factor-k B (NF-kB) signaling pathways
The OVA sensitization and airway challenges induced remarkable increases in the levels of T helper 2 (TH2) cytokines, including IL-4, IL-5, and IL-13,in Bronchoalveolar Lavage Fluid (BALF) compared with the sham group (Fig. 2)
Summary
Allergic asthma is a chronic airway inflammatory disease that affects over 300 million people worldwide [1]. Activation of allergen-specific T helper 2 (TH2) cells releases cytokines to induce B cells (via IL-4 and IL-13) and to promote eosinophil maturation (via IL-5) [4,5,6]. Well-established therapies for allergic asthma mainly include inhaled corticosteroids and b-adrenergic receptor agonists. Corticosteroids take effect by suppressing the expression of inflammatory genes such as nuclear factor-k B (NF-kB), which is activated during inflammatory responses to increase expression levels of cytokines, chemokines, and adhesion molecules [9,10]. Inhaled b-adrenergic agonists are effective bronchodilators that mainly relax airway smooth muscle and quickly relieve asthma symptoms [11,12]. Developments of new therapeutic intervention are needed as alternative or supplement to current asthma treatments
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