Abstract
Mangiferin is a major bioactive ingredient in Mangifera indica Linn. (Anacardiaceae) leaves. Aqueous extract of such leaves have been used as an indigenous remedy for respiratory diseases like asthma and coughing in traditional Chinese medicine. However, underlying molecular mechanisms of mangiferin on anti-asthma remain unclear. In our present study, we investigated the anti-asthmatic effect of mangiferin on Th1/Th2 cytokine profiles and explored its underlying immunoregulatory mechanism in mouse model of allergic asthma. Mangiferin significantly reduced the total inflammatory cell counts and eosinophil infiltration, decreased the production of ovalbumin-specific IgE in serum and PGD2 in BALF. The antibody array analysis showed that mangiferin down-regulated the levels of one group of cytokines/chemokines including Th2-related IL-4, IL-5, IL-13, and others IL-3, IL-9, IL-17, RANTES, TNF-α, but simultaneously up-regulated Th1-related IFN-γ, IL-2 and IL-10 and IL-12 expression in serum. Thus it attenuates the imbalance of Th1/Th2 cells ratio by diminishing the abnormal mRNA levels of Th1 cytokines (IFN-γ and IL-12) and Th2 cytokines (IL-4, IL-5 and IL-13). Finally, mangiferin substantially inhibited the activation and expression of STAT-6 and GATA-3 in excised lung tissues. Our results suggest that mangiferin can exert anti-asthmatic effect. The underlying mechanism may attribute to the modulation of Th1/Th2 cytokine imbalance via inhibiting the STAT6 signaling pathway.
Highlights
Allergic asthma is a chronic inflammatory disease of the bronchial airways characterized by infiltrating of a variety of inflammatory cells, including eosinophils, mast cells, T-lymphocytes, neutrophils, and macrophages among others [1]
We found that the levels of phosphorylated STAT6 (p-STAT6) and GATA-binding protein-3 (GATA-3) in the lung tissues were markedly inhibited by mangiferin
We demonstrated that mangiferin inhibited OVAinduced asthmatic response by reducing airway inflammation, prostaglandin D2 (PGD2) production and OVA-specific IgE level
Summary
Allergic asthma is a chronic inflammatory disease of the bronchial airways characterized by infiltrating of a variety of inflammatory cells, including eosinophils, mast cells, T-lymphocytes, neutrophils, and macrophages among others [1]. The incidence and severity of atopic disorders has steadily increased in developed countries [2]. Th2 cell responses initiate and predominate in atopic disorders through releasing of Th2 cytokines, mainly IL-4, IL-5 and IL-13, which elevate the serum immunoglobulin E and recruit eosinophils to airways, further inducing secretion of histamine, leukotriene and prostaglandin. Immune responses of Th1 and Th2 cells maintain dynamic balance. Whenever this balance is disturbed, diseases will occur. One effective treatment for asthma is to try to improve Th1 immune responses and simultaneously inhibit Th2 immune responses to restore Th1/Th2 balance [4]
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