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-1β, IL-6, and TNF-α 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-κB 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-κB signaling pathway, which may likely serve as a novel therapeutic drug for AD management.

中文翻译：

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光甘草定通过下调 TLR4/MyD88/NF-κB 信号通路减缓特应性皮炎进展

背景

光甘草定 (GB) 是一种生物可利用的植物雌激素，具有抗炎、抗菌和抗病毒等多种生物学特性。

客观的

探讨GB在特应性皮炎（AD）过程中的作用。

方法

CCK8用于检测光甘草定在HaCat和NHEK细胞炎症模型中的治疗作用。并评估对细胞增殖和细胞活力的影响。qRT-PCR和PCR检测HaCat和NHEK细胞组织中TLR4、MyD88、P65和P50的表达。同时构建AD动物模型，通过苏木精-伊红（HE）和免疫组化染色（IHC）验证细胞实验结果。

结果

酶联免疫吸附试验 (ELISA) 表明，通过 GB 处理，脂多糖 (LPS) 上调的 IL-1β、IL-6 和 TNF-α 降低。通过实时 PCR 和蛋白质印迹分析，通过抑制 TLR4/MyD88/NF-κB 信号通路进一步证实了 AD 进展受 GB 的调节。AD 样小鼠模型表明，通过 H&E 染色，GB 可显着减轻表皮损伤、减轻水肿并减少炎症细胞浸润。同时，IHC 染色显示 GB 通过阻止 TLR4 表达来减少 AD 进展。

结论

观察到 GB 通过抑制 TLR4/MyD88/NF-κB 信号通路来降低 AD 进展，这可能作为一种新的 AD 治疗药物。