Water Extract of Inula japonica Flower Ameliorates Dermatophagoides farinae Extract-Induced Atopic Dermatitis-like Skin Inflammation by Attenuating JAK/STAT Signaling.

日本旋覆花水提取物通过减弱 JAK/STAT 信号传导来改善粉尘螨提取物引起的特应性皮炎样皮肤炎症

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作者:Shim Ki-Shuk, Kim Hye Jin, Gu Dong Ryun, Kim Seong Cheol, Lee Ik Soo, Chae Sung-Wook, Park Musun, Kim Taesoo, Kim Ki Mo
The Inula japonica flower is traditionally used to alleviate lung inflammatory symptoms. While the therapeutic effect of the I. japonica flower on lung diseases has been suggested, the efficacy of the I. japonica flower in treating atopic dermatitis (AD) remains unknown. We investigated the effects of a water extract of the I. japonica flower (WEIF) on Dermatophagoides farinae extract (DfE)-induced AD-like inflammation in NC/Nga mice. Histological analysis of the epidermal structure, mast cell infiltration, and barrier protein expression were examined. Serum inflammatory mediator levels were assessed. To elucidate the regulatory pathway of WEIF, the effects of 1,5-dicaffeoylquinic acid (DCQA) and 1-O-acetylbritannilactone (ABL) in WEIF on the JAK/STAT pathway were evaluated in interferon-γ/tumor necrosis factor (TNF)-α-stimulated human adult epidermal keratinocytes. WEIF ameliorated DfE-induced skin inflammation by reducing dermatitis scores, mast cell infiltration, skin structural damage, and serum inflammatory mediator levels. Additionally, DCQA and ABL significantly inhibited JAK/STAT activation in interferon-γ/TNF-α-treated keratinocytes. Furthermore, ligand-binding analysis revealed high binding affinities of DCQA and ABL for JAK. These results suggest the pharmacological potential of WEIF to alleviate DfE-induced skin inflammation by inhibiting the JAK/STAT signaling pathway. In conclusion, these findings support the development of WEIF as a therapeutic treatment for AD-like skin inflammatory diseases.

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