Anti-inflammatory effects and immunomodulatory mechanisms of myricetin in atopic dermatitis
學生姓名:
余之曦
指導教授:
黃崇雄
學期:
114下
摘 要:
Atopic dermatitis (AD) is a chronic and recurrent inflammatory skin disease characterized by skin dryness, erythema, eczema, pruritus, and desquamation, and severe cases may involve skin thickening and crust formation. Its development is closely associated with immune imbalance, inflammatory responses, and impaired skin barrier function. Myricetin (Myr), a natural flavonoid compound, possesses anti-inflammatory and immunomodulatory activities. Therefore, this study integrates two related studies to investigate its therapeutic effects on AD and its potential mechanisms. The results showed that myricetin alleviated calcipotriol (MC903)-induced AD-like symptoms and reduced inflammatory and allergic response indicators by inhibiting the expression of Interleukin-4 (IL-4), Interferon-gamma (IFN-γ), Thymus and Activation-Regulated Chemokine (TARC), and Thymic Stromal Lymphopoietin (TSLP), while upregulating filaggrin (FLG). In HaCaT cells, myricetin also reduced the expression of TARC and Macrophage-Derived Chemokine (MDC), while suppressing the activation of STAT1 and NF-κB signaling pathways. In addition, in 2,4-Dinitrochlorobenzene (DNCB)-induced AD mice and RAW264.7 macrophage polarization models, myricetin regulated macrophage M1/M2 polarization, decreased M1-related pro-inflammatory markers, and increased M2-related repair markers, thereby suppressing inflammation and promoting tissue repair. Overall, myricetin may improve AD pathological changes through multiple mechanisms, including immune balance regulation, skin barrier repair, and macrophage polarization modulation, suggesting its potential as a natural therapeutic candidate for atopic dermatitis.
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