Glabridin attenuates atopic dermatitis progression through downregulating the TLR4/MyD88/NF-κB signaling pathway

Background Glabridin (GB), a bio-available phytoestrogen, displays various biological properties such as anti-inflammatory, antibacterial, and antiviral. Objective To explore the role of GB in the process of atopic dermatitis (AD). Methods CCK8 was used to detect the therapeutic effect of Glabridin in HaCat and NHEK cell inflammatory models. And evaluated the effect on cell proliferation and cell viability. The expression of TLR4, MyD88, P65 and P50 in HaCat and NHEK cell tissues was detected by qRT-PCR and PCR. At the same time, an AD animal model was constructed, and the cell experiment results were verified by hematoxylin-eosin (HE) and Immunohistochemistry staining (IHC). Results Enzyme-linked immunosorbent assay (ELISA) demonstrated that IL-1 beta, IL-6, and TNF-alpha upregulated by lipopolysaccharide (LPS) was decreased by treatment with GB. AD progression was further confirmed to be regulated by GB by inhibiting the TLR4/MyD88/NF-kappa B signaling pathway through real-time PCR and Western blot analyses. An AD-like mouse model demonstrated that GB considerably alleviated epidermal injury, relieve edema, and reduced inflammatory cell infiltration by H&E staining. Concurrently, IHC staining exhibited GB to reduce AD progression by impeding TLR4 expression. Conclusion GB was observed to decrease the AD progression by suppressing the TLR4/MyD88/NF-kappa B signaling pathway, which may likely serve as a novel therapeutic drug for AD management.