Journal of ethnopharmacology · 2026
Tuihong formula attenuates DNCB-induced atopic dermatitis in mice via suppression of MAPK/NF-κB signaling and epidermal barrier restoration.
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Huang Yingqi, Lin Weijun, Chen Xiaoyan, Lin Fuyuan, Li Jiajie, Liu Yaosheng, Liu Yumei, Luo Guangpu, Du Xianhua, Duan Lixin, Zhan Yaxian, Zhao Tie
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: The Tuihong Formula (THF) has been used in traditional Chinese folk medicine as a topical herbal preparation for the treatment of cutaneous disorders, and its therapeutic efficacy is well established. Although THF has shown promising clinical efficacy in atopic dermatitis (AD), but its pharmacological mechanisms remain unclear.
AIM OF THE STUDY: This study aims to explore THF's potential mechanisms in AD and provide experimental evidence for its treatment.
MATERIALS AND METHODS: An AD-like skin inflammation model was established in mice using 2,4-dinitrochlorobenzene (DNCB). After successful modeling, THF was applied topically. Daily body weight, skin lesion scores and skin thickness were recorded. Stain the skin tissue samples with (H&E) and toluidine blue, observe the changes in their microstructure, and count the number of mast cells. Laser speckle imaging evaluated skin perfusion. A comprehensive assessment included skin barrier function (TEWL, occludin, AQP3, TSLP, TRPV1), spleen index, Th1/Th2 ratio, serum IgE, and inflammatory cytokines (TNF-α, IL-4, IL-1β), using non-invasive skin analyzers, immunohistochemistry, ELISA, qRT-PCR, flow cytometry, and Western blot. To evaluate potential corticosteroid-like side effects, THF and various corticosteroids were applied long-term to normal mice, with monitoring of skin condition, body weight, lesion scores and skin thickness. Skin and major organs were collected for analysis.
RESULTS: THF effectively improved AD-like lesions in mice. It reduced epidermal thickness and decreased mast cell and degranulated mast cell numbers. Serum IgE, IL-4, and TNF-α levels were lowered, while occludin expression increased. THF modulated the Th1/Th2 balance in the spleen, downregulating organ indices. RT-qPCR showed elevated IL-4 and IL-1β in AD-like lesions. Western blot confirmed that THF reduced phosphorylation of ASK1, p38, JNK, c-Jun, p65, IKK and IκBα. Safety evaluation indicated long-term THF use did not alter body weight, skin thickness, or structure and caused no organ damage, demonstrating high safety without corticosteroid-like adverse effects.
CONCLUSION: THF alleviates DNCB-induced AD in mice by modulating inflammation, repairing the skin barrier, regulating Th1/Th2 balance, and inhibiting MAPK/NF-κB pathways. Furthermore, THF demonstrates a favorable safety profile for long-term topical application. This study supports further exploration of traditional Chinese medicine topical formulations for AD treatment.
AIM OF THE STUDY: This study aims to explore THF's potential mechanisms in AD and provide experimental evidence for its treatment.
MATERIALS AND METHODS: An AD-like skin inflammation model was established in mice using 2,4-dinitrochlorobenzene (DNCB). After successful modeling, THF was applied topically. Daily body weight, skin lesion scores and skin thickness were recorded. Stain the skin tissue samples with (H&E) and toluidine blue, observe the changes in their microstructure, and count the number of mast cells. Laser speckle imaging evaluated skin perfusion. A comprehensive assessment included skin barrier function (TEWL, occludin, AQP3, TSLP, TRPV1), spleen index, Th1/Th2 ratio, serum IgE, and inflammatory cytokines (TNF-α, IL-4, IL-1β), using non-invasive skin analyzers, immunohistochemistry, ELISA, qRT-PCR, flow cytometry, and Western blot. To evaluate potential corticosteroid-like side effects, THF and various corticosteroids were applied long-term to normal mice, with monitoring of skin condition, body weight, lesion scores and skin thickness. Skin and major organs were collected for analysis.
RESULTS: THF effectively improved AD-like lesions in mice. It reduced epidermal thickness and decreased mast cell and degranulated mast cell numbers. Serum IgE, IL-4, and TNF-α levels were lowered, while occludin expression increased. THF modulated the Th1/Th2 balance in the spleen, downregulating organ indices. RT-qPCR showed elevated IL-4 and IL-1β in AD-like lesions. Western blot confirmed that THF reduced phosphorylation of ASK1, p38, JNK, c-Jun, p65, IKK and IκBα. Safety evaluation indicated long-term THF use did not alter body weight, skin thickness, or structure and caused no organ damage, demonstrating high safety without corticosteroid-like adverse effects.
CONCLUSION: THF alleviates DNCB-induced AD in mice by modulating inflammation, repairing the skin barrier, regulating Th1/Th2 balance, and inhibiting MAPK/NF-κB pathways. Furthermore, THF demonstrates a favorable safety profile for long-term topical application. This study supports further exploration of traditional Chinese medicine topical formulations for AD treatment.