Astilbin Ameliorates Atopic Dermatitis via Modulation of miR-31-5p

Abstract

Previous studies have reported the potential role of astilbin (AL) in skin lesions and the abnormal expression of miR-31-5p in the skin of patients with atopic dermatitis (AD). To elucidate the efficacy of AL in improving AD and to determine whether its molecular mechanism is associated with miR-31-5p. Serum miR-31-5p levels were measured via reverse transcription quantitative polymerase chain reaction (RT-qPCR) in 32 AD patients and 25 healthy controls. A 2,4-dinitrofluorobenzene (DNFB)-induced AD mice model was established to evaluate AL’s therapeutic effects using dermatitis/erythema scores, itching behavior, and serum immunoglobulin E (IgE)/inflammatory factor levels measured by enzyme-linked immunosorbent assay (ELISA). An in vitro AD model using tumor necrosis factor-α/interferon-γ (TNF-α/IFN-γ)-stimulated human keratinocyte (HaCaT) cells was established. The impact of AL on cell viability and inflammatory factors was analyzed using cell counting kit-8 (CCK-8) and ELISA. Rescue experiments assessed the miR-31-5p regulatory mechanism. Serum miR-31-5p was significantly upregulated in AD patients and model mice. AL alleviated AD symptoms dose-dependently by reducing serum IgE and inflammatory cytokines (TNF-α, IL-4 (interleukin-4), IL-6 (interleukin-6), IL-1β (interleukin-1β)). AL suppressed TNF-α/IFN-γ-induced miR-31-5p overexpression in HaCaT cells, improved cell viability, and reduced inflammatory factor secretion. These effects were partially reversed by a miR-31-5p mimic. AL significantly improves AD, potentially by inhibiting miR-31-5p expression to reduce inflammatory responses and improve keratinocyte function. This study reveals a pharmacological role for AL and provides a novel therapeutic target for AD.