# Chaga Mushroom (Inonotus obliquus) Attenuates DNCB-Induced Atopic Dermatitis by Modulating Oxidative Stress and Cytokine Expression

## TL;DR

Chaga mushroom extract may help treat atopic dermatitis by reducing inflammation and oxidative stress.

## Contribution

The study demonstrates the therapeutic potential of a Chaga mushroom by-product in managing atopic dermatitis.

## Key findings

- E-CME treatment improved dermatitis scores and reduced mast cell infiltration in mice.
- E-CME modulated serum immunoglobulin levels and oxidative stress markers.
- E-CME enhanced splenocyte viability and reduced inflammatory cytokine expression.

## Abstract

Recent studies highlight the immunomodulatory properties of Chaga mushrooms. Atopic dermatitis (AD) is a multifactorial skin disorder involving interactions between innate and adaptive immune responses. This investigation evaluates the anti-atopic dermatitis activity of a by-product from ethanol-extracted Chaga mushroom (E-CME), positioning it as a sustainable natural candidate for AD therapeutic development. The antioxidant potential of E-CME was assessed using DPPH radical scavenging, H2O2 scavenging, metal chelation, and FRAP assays. In vitro, its immunomodulatory effects were evaluated in HaCaT and RBL-2H3 cell lines by measuring cytokine release and β-Hexosaminidase activity. For in vivo analysis, E-CME was topically applied to BALB/c mice sensitized with Dermatophagoides farinae extract (DFE), with AD induced by DNCB. Post-treatment, inflammatory cytokine expression and MAPK marker expression were examined. E-CME treatment significantly improved dermatitis scores (p < 0.05), mast cell infiltration, serum immunoglobulin levels (24.07% increase of IgG2, 26.19% decrease of IgE), oxidative stress markers, and skin cytokine gene expression. Spleen and lymph node weights, plus splenocyte viability, also improved with E-CME treatment. These findings suggest that E-CME possesses substantial therapeutic potential for AD management, attributed to its antioxidant and immunomodulatory effects, possibly mediated by the inhibition of oxidative stress-associated inflammatory pathways.