Mangiferin can alleviate atopic dermatitis-like responses in mice and HaCaT cells

BackgroundAtopic dermatitis (AD) is a chronic inflammatory disorder that can affect the physical and psychological health of individuals worldwide. Mangiferin has been previously shown to alleviate allergic diseases.ObjectivesTo investigate the effect of mangiferin on AD-like pathologies and the mechanism of action.MethodsAfter establishing a mouse model of AD by challenging male BALB/c mice with 1% 2,4-dinitrochlorobenzene (DNCB), 10, 50, and 100 mg/kg mangiferin was administered orally for 21 days. Scratching behaviors, dermatitis score, spleen weight, and serum immunoglobulin E (IgE) levels were assessed. Histopathological changes were determined using toluidine blue and hematoxylin-eosin staining. A cellular model of AD was established by co-stimulating HaCaT keratinocytes with tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma. The mRNA expression of chemokines and Th2-related cytokines was examined using RT-qPCR. Western blot and immunofluorescence were used to detect the protein levels of markers of the AKT/NF-kappa B/STAT1 and MAPK pathways.ResultsMangiferin exhibited anti-atopic effects in DNCB-induced AD-like mice as evidenced by decreased scratching behaviors, dermatitis score, spleen weight, IgE levels, skin thickness, and mast cell infiltration in mice. Additionally, mangiferin inhibited expression of chemokines and Th2 type cytokines (IL-4, IL-5, and IL-13) in AD-like mice and TNF-alpha/IFN-gamma-co-stimulated HaCaT cells. Moreover, mangiferin attenuated TNF-alpha/IFN-gamma-induced release of various inflammatory factors (such as TNF-alpha, IL-1 beta, and IL-6) in HaCaT cells. Mangiferin repressed the activation of the AKT/NF-kappa B/STAT1 and MAPK signaling pathways under both in vivo and in vitro conditions.ConclusionOverall, mangiferin inhibits the inflammatory and pruritic responses in AD, which might be an effective drug for AD treatment.