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Background <p>Atopic dermatitis (AD) is one of the most common chronic, persistent, recurrent, and inflammatory skin diseases, commonly known as atopic eczema. <i>Drynariae rhizome</i> (DR) is commonly used to treat inflammation, osteoporosis, hyperlipidemia, and alopecia areata. However, there is no research report on the treatment of AD skin inflammation with DR water extract (WDR).</p> Objective <p>This study aims to investigate the therapeutic effect of WDR on 2,4-dinitrochlorobenzene (DNCB)-induced AD mouse model and explore its molecular mechanism.</p> Results <p>A large number of lichenified skin lesions, redness, and scales could be observed on the back skin of mice in the DNCB group; H&amp;E staining and toluidine blue staining results showed abnormal hyperplasia of the epidermis and dermis in the skin lesions, and the number of infiltrated mast cells in the dermis was increased; immunohistochemistry (IHC) results showed that the expression levels of iNOS, CD86, CD163, and CD206 in the skin lesions were increased; Western blot results showed that the protein expression levels of IL-17, Keap1, p-NF-κB p65, and p-JNK were increased and the protein expression levels of Nrf2 and HO-1 were decreased significantly in the skin lesions (<i>p</i> &lt; 0.001, <i>p</i> &lt; 0.05). There were only a few lichenified lesions on the back skin of mice in each dexamethasone (DXMS) or WDR treatment group, the abnormal hyperplasia of epidermis and dermis in lesional tissue was reduced, the number of infiltrating mast cells in dermis was significantly reduced, the protein expression levels of iNOS and CD86 were decreased and the levels of CD163 and CD206 was increased in varying degrees in lesional tissue, the protein expression levels of IL-17, Keap1, p-NF-κB p65, p-JNK in lesional tissue were significantly decreased, and the protein expression levels of Nrf2 and HO-1 were significantly were increased, especially in the WDR high-dose group (<i>p</i> &lt; 0.05).</p> Conclusions <p>WDR can treat AD by regulating oxidative stress and MAPK and NF-κB signaling pathways.</p>

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Therapeutic effect of Drynariae rhizoma water extract on DNCB-induced atopic dermatitis in mice

  • 期刊论文

  • 发表日期：

    2026年5月12日

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  • CaoYue Yu,
  • YaoZi Wang,
  • YiMing Hu,
  • YueNan Wang,
  • WenLe Zhang,
  • QianNi Xiao,
  • XiangYu You

摘要

Background

Atopic dermatitis (AD) is one of the most common chronic, persistent, recurrent, and inflammatory skin diseases, commonly known as atopic eczema. Drynariae rhizome (DR) is commonly used to treat inflammation, osteoporosis, hyperlipidemia, and alopecia areata. However, there is no research report on the treatment of AD skin inflammation with DR water extract (WDR).

Objective

This study aims to investigate the therapeutic effect of WDR on 2,4-dinitrochlorobenzene (DNCB)-induced AD mouse model and explore its molecular mechanism.

Results

A large number of lichenified skin lesions, redness, and scales could be observed on the back skin of mice in the DNCB group; H&E staining and toluidine blue staining results showed abnormal hyperplasia of the epidermis and dermis in the skin lesions, and the number of infiltrated mast cells in the dermis was increased; immunohistochemistry (IHC) results showed that the expression levels of iNOS, CD86, CD163, and CD206 in the skin lesions were increased; Western blot results showed that the protein expression levels of IL-17, Keap1, p-NF-κB p65, and p-JNK were increased and the protein expression levels of Nrf2 and HO-1 were decreased significantly in the skin lesions (p < 0.001, p < 0.05). There were only a few lichenified lesions on the back skin of mice in each dexamethasone (DXMS) or WDR treatment group, the abnormal hyperplasia of epidermis and dermis in lesional tissue was reduced, the number of infiltrating mast cells in dermis was significantly reduced, the protein expression levels of iNOS and CD86 were decreased and the levels of CD163 and CD206 was increased in varying degrees in lesional tissue, the protein expression levels of IL-17, Keap1, p-NF-κB p65, p-JNK in lesional tissue were significantly decreased, and the protein expression levels of Nrf2 and HO-1 were significantly were increased, especially in the WDR high-dose group (p < 0.05).

Conclusions

WDR can treat AD by regulating oxidative stress and MAPK and NF-κB signaling pathways.