Glabridin ameliorates DNFB induced atopic dermatitis by suppressing MAPK/NF κB signaling pathways in mice

Abstract

Purpose: To investigate the anti-inflammatory mechanism of action of glabridin (GBD) isolated from glycyrrhizae radix et rhizoma (Glycyrrhiza glabra L.) using atopic dermatitis (AD) mouse model. Methods: Nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways were investigated. The dorsal skin and serum of 2,4-dinitrofluorobenzene (DNFB)-induced AD mice were used to determine the levels of various inflammatory cytokines, including interferon (IFN)-γ, tumor necrosis factor (TNF)-α, interleukin (IL)-4, IL-5, IL-6, IL-13, and immunoglobulin E (IgE) by enzyme-linked immunosorbent assay (ELISA). The relative levels of inflammation-associated mRNA and signaling pathways were determined by real time-polymerase chain reaction (RT-PCR) and western blotting, respectively. Hematoxylin and eosin (H&E) staining was used to assess the effect of GBD on tissue thickening and inflammatory cell infiltration in mice with AD. Results: Glabridin significantly relieved dorsal skin thickening, scabbing, and bleeding, and reduced the infiltration of inflammatory cells in mice with AD (p < 0.05). The levels of IFN-γ, TNF-α, IL-4, IL-5, IL-6, IL-13, and IgE were significantly reduced (p < 0.05 or 0.01). Moreover, the relative levels of IL-6 and IFN-γ mRNA showed a significant decrease (p < 0.01). Furthermore, GBD inhibited phosphorylation of MAPK signaling pathway and activation of NF-κB (p < 0.05 or 0.01). Conclusion: Glabridin exerts an inhibitory effect on AD by blocking MAPK and NF-κB signaling pathways. This finding highlights the relationship between traditional Chinese medicine and modern AD therapeutic methods, which should be further investigated for its potential to be developed as an external anti-AD medicine.