Zhu Congcong, Wu Junchao, Chen Ya, Ma Tianyou, Pan Huijun, Zhai Chuntao, Tai Zongguang, Chen Zhongjian, Zhu Quangang
Shanghai Skin Disease Hospital, School of Medicine, Tongji University, 1278 Baode Road, Shanghai, 200443, China.
Shanghai Engineering Research Center for Topical Chinese Medicine, 1278 Baode Road, Shanghai, 200443, China.
Mol Cell Biochem. 2025 May 20. doi: 10.1007/s11010-025-05270-7.
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.
白菊精华（BJE）是一种由药用植物提取物组成的生物活性制剂，因其治疗潜力而被用于护肤品中。特应性皮炎（AD）是一种慢性炎症性皮肤病，其特征为表皮屏障功能障碍和免疫失调。本研究旨在评估BJE的抗炎和皮肤保护作用及其治疗AD的潜在机制。在HaCaT细胞中评估BJE恢复表皮屏障的能力。在脂多糖（LPS）诱导的RAW264.7细胞中，通过测量一氧化氮（NO）、白细胞介素-6（IL-6）、前列腺素E2（PGE2）和肿瘤坏死因子-α（TNF-α）来评估BJE的抗炎潜力。采用蛋白质免疫印迹分析来评估丝裂原活化蛋白激酶（MAPK）途径的调控。使用MC903建立体内类AD小鼠模型，并记录体重、耳厚度和AD症状的测量值。组织学分析对肥大细胞浸润进行定量，而蛋白质免疫印迹法测定丝聚蛋白（FLG）、兜甲蛋白（LOR）和脂肪酸延长酶6（ELOVL6）的表达。酶联免疫吸附测定（ELISA）用于测量TNF-α、免疫球蛋白E（IgE）、IL-4和IL-13水平。流式细胞术评估BJE对辅助性T细胞（Th）表型的影响。BJE显著增强了HaCaT细胞中皮肤屏障蛋白的表达（神经酰胺2（CERS2）、LOR、透明质酸合成酶-1（HAS-1）、透明质酸合成酶-2（HAS-2）、FLG）。它显著降低了LPS处理的RAW264.7细胞中NO、IL-6、PGE2和TNF-α的水平，证明了其抗炎潜力。从机制上讲，BJE抑制MAPK激活。BJE降低了类AD小鼠的耳厚度，改善了皮肤损伤，并缓解了AD症状。此外，BJE有效抑制了肥大细胞浸润和角化过度。BJE还降低了TNF-α、IgE、IL-4和IL-13的水平，同时增加了LOR、ELOVL6和FLG的表达。此外，BJE调节了Th1、Th2和Th17细胞的比例。BJE促进了HaCaT细胞中表皮屏障的修复，抑制了RAW264.7细胞中LPS诱导的炎症，增强了类AD小鼠的皮肤屏障完整性，并通过恢复Th细胞平衡发挥免疫调节作用。这些发现突出了BJE通过其抗炎和皮肤屏障修复的双重作用在AD治疗中的潜力。
