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Managing atopic dermatitis through the perspectives of "clear-turbid interference" and the "gut-skin axis"
Journal of Beijing University of Traditional Chinese Medicine 2025, 48(10): 1413-1418
Published: 29 September 2025
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Atopic dermatitis is a common chronic, relapsing, inflammatory skin disease; however, its pathogenesis remains unclear. The theory of "clear-turbid interference" originates from the Inner Canon of Yellow Emperor and refers to a pathological condition in which clear yang and turbid yin intermingle, and qi movement becomes disordered. This paper elucidates the theoretical connotation of "clear-turbid interference" and its core mechanism in triggering atopic dermatitis, as well as the role of the "gut-skin axis" in atopic dermatitis development. Internal dampness-turbidity and disharmony between ying and wei constitute the core pathological mechanisms linking clear-turbid interference to atopic dermatitis. Treatment for different stages and syndromes should be guided by syndrome differentiation. For example, for spleen deficiency with a dampness syndrome in subacute or chronic stages, Chushi Weiling Decoction may be used to fortify the spleen, eliminate dampness, lift the clear, and downbear the turbid. For patterns with prominent heat manifestations, such as dampness-heat immersion or heart fire with spleen deficiency, bitter-cold dampness-drying herbs can be added on this basis. For wind-dampness-heat accumulation in the acute stage, Mahuang Lianyao Chixiaodou Decoction can be used to release the exterior, expel pathogens, and harmonize ying and wei. In cases of spleen deficiency with blood dryness or liver-kidney insufficiency during the chronic stage, in addition to nourishing yin to moisten the skin and tonifying the liver-kidney, wind-medicinals should also be employed to open the sweat pores and promote qi movement. These approaches restore the physiological state without clear-turbid interference while regulating intestinal flora, providing new approaches and perspectives for integrating traditional Chinese and Western medicine in treating atopic dermatitis.

Open Access Original Article Issue
Exploring the effect of Mahuang Lianqiao Chixiaodou decoction on NLRP3 cell pyroptosis in an atopic dermatitis-like mouse model
Journal of Traditional Chinese Medical Sciences 2023, 10(4): 461-469
Published: 25 September 2023
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Objective

To investigate the efficacy and mechanism of Mahuang Lianqiao Chixiaodou decoction (MLCD) in intervening in the “internal and external crosstalk” between skin barrier dysfunction and immune inflammation in an atopic dermatitis-like (AD-like) mouse model via the NOD-like receptor protein 3 (NLRP3) pyroptosis pathway.

Methods

AD-like model mice were induced with 2,4-dinitrofluorobenzene and treated with MLCD or mometasone furoate gel (MF, positive control) for 7 days. Pathological changes in skin tissue were examined using Masson or methamphetamine blue staining. A smart skin analyzer, flow cytometry, fluorescence quantitative polymerase chain reaction, and western blotting were used to observe and evaluate skin barrier dysfunction, immune inflammatory responses, and skin cell pyroptosis in AD-like mice.

Results

MLCD and MF improved skin damage and reduced pathological tissue damage and mast cell infiltration in AD-like mice to varying degrees. MLCD significantly reduced skin pigmentation and inflammatory status (P =.005 and P =.038, respectively), increased the percentage of splenic CD4+CD3+ T cells (P =.022), decreased the CD8+CD3+ T cell percentage (P =.044), decreased the CD8+CD3+/CD3+ ratio (P =.031) and increased the CD4+CD3+/CD8+CD3+ ratio (P =.027). MLCD also significantly decreased the mRNA expression levels of cell scorch-related factors NLRP3, casp-1, interleukin (IL)-1β, and IL-18 (P =.027, P <.001, P =.012, and P =.039, respectively), as well as the protein expression of NLRP3, casp-1, apoptosis-associated speck-like protein containing a CARD, and IL-1β (P =.002, P =.006, P =.004, and P =.035, respectively).

Conclusion

MLCD achieved efficacy in the treatment of AD-like mice by interfering with the “internal and external crosstalk” mechanisms of skin barrier dysfunction and immune inflammation mediated by NLRP3 pyroptosis.

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