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

## TL;DR

A water extract from Inula japonica flowers reduces skin inflammation in a mouse model of atopic dermatitis by inhibiting the JAK/STAT signaling pathway.

## Contribution

The study identifies the anti-inflammatory effects of Inula japonica flower extract and its active compounds on atopic dermatitis via JAK/STAT pathway inhibition.

## Key findings

- WEIF reduced dermatitis scores, mast cell infiltration, and skin damage in mice.
- DCQA and ABL inhibited JAK/STAT activation in keratinocytes.
- DCQA and ABL showed high binding affinity for JAK proteins.

## Abstract

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.