ArticleMolecular and cellular biochemistry2025
The alleviating effect of Bai-Ju essence on atopic dermatitis through anti-inflammatory and skin barrier repair mechanisms.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Translational insights into interleukin-driven macrophage polarization as diagnostic biomarkers for atopic dermatitis-a narrative review.Frontiers in molecular biosciences · 2026Review
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9 authors.
Funding
Abstract
Bai-Ju essence (BJE) is a bioactive formulation composed of medicinal plant extracts, utilized in skincare products for its therapeutic potential. Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by epidermal barrier dysfunction and immune dysregulation. This study aimed to evaluate BJE anti-inflammatory and skin-protective effects, and its potential mechanisms in treating AD. The ability of BJE to restore the epidermal barrier was assessed in HaCaT cells. In LPS-induced RAW264.7 cells, the anti-inflammatory potential of BJE was evaluated by measuring NO, IL-6, PGE2, and TNF-α. Western blot analysis was used to assess the regulation of the MAPK pathway. An in vivo AD-like mouse model was established using MC903, and measurements of body weight, ear thickness, and AD symptoms were recorded. Histological analysis quantified mast cell infiltration, while western blot determined FLG, LOR, and ELOVL6 expression. ELISA was used to measure TNF-α, IgE, IL-4, and IL-13 levels. Flow cytometry assessed the effect of BJE on Th cell phenotypes. BJE significantly enhanced skin barrier protein expression (CERS2, LOR, HAS-1, HAS-2, FLG) in HaCaT cells. It significantly reduced the levels of NO, IL-6, PGE2, and TNF-α in LPS-treated RAW264.7, demonstrating its anti-inflammatory potential. Mechanistically, BJE inhibited MAPK activation. BJE decreased ear thickness, improved skin lesions, and relieved AD symptoms in AD-like mice. In addition, BJE effectively suppressed mast cell infiltration and hyperkeratosis. BJE also decreased levels of TNF-α, IgE, IL-4, and IL-13 while increasing LOR, ELOVL6, and FLG expressions. Furthermore, BJE modulated Th1, Th2, and Th17 cell proportions. BJE promoted epidermal barrier repair in HaCaT, suppressed the LPS-induced inflammation in RAW264.7, enhanced the skin barrier integrity in AD-like mice, and exhibited immunomodulatory effects by restoring Th cell balance. These findings highlighted the therapeutic potential of BJE in AD through its dual action of anti-inflammation and skin barrier restoration.
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