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日用化学工业（中英文）

日用化学工业（中英文） ›› 2026, Vol. 56 ›› Issue (5): 603-613.doi: 10.3969/j.issn.2097-2806.2026.05.007

• 基础研究 • 上一篇    下一篇

基于Nrf2/TLR4信号通路的低聚木糖皮肤防护功效原料开发、功效及机制研究

张瑞敏1,张磊2,*(),何亚飞1,范丽敏1   

  1. 1.濮阳医学高等专科学校，河南 濮阳 457000
    2.北京中日友好医院，北京 100029
  • 收稿日期:2026-01-13 修回日期:2026-04-21 出版日期:2026-05-22 发布日期:2026-06-22
  • 基金资助:
    2025年度河南省高校人文社会科学研究一般项目(2025-ZZJH-128)

Research on development, efficacy and mechanism of xylooligosaccharides as a skin protective functional ingredient based on the Nrf2/TLR4 signaling pathway

Ruimin Zhang1,Lei Zhang2,*(),Yafei He1,Limin Fan1   

  1. 1. Puyang Medical College, Puyang, Henan 457000, China
    2. China-Japan Friendship Hospital, Beijing 100029, China
  • Received:2026-01-13 Revised:2026-04-21 Online:2026-05-22 Published:2026-06-22
  • Contact: *E-mail: zhanglei1122334@126.com.

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摘要： 研究低聚木糖（XOS）对皮肤屏障免疫功能的调控作用及分子机制，通过构建紫外线B（UVB）诱导损伤与金黄色葡萄球菌培养上清液（SA-CS）诱导炎症两种HaCaT细胞模型开展系统研究。UVB损伤模型中，HaCaT细胞经30 mJ/cm2 UVB照射后使用XOS低、中、高剂量（50，100，200 μg/mL）及Nrf2抑制剂ML385处理24 h；SA-CS炎症模型中，细胞经20% SA-CS处理24 h，同时在培养基中添加XOS低、中、高剂量及TLR4激动剂（LPS），每组均设6个复孔。检测细胞存活率、凋亡率（TUNEL法）、凋亡相关基因（Bax、Bcl-2） mRNA水平、跨膜电阻（TEER）值、屏障相关蛋白（FLG、Claudin-1/4） mRNA水平、氧化应激指标（ROS、MDA、SOD）、Nrf2/Keap1通路蛋白、炎症因子（IL-1β、IL-8、TNF-α等）及TLR4/NF-κB通路蛋白水平。结果显示：UVB照射显著降低HaCaT细胞存活率与TEER值，下调屏障相关蛋白mRNA表达，促进细胞凋亡，引发氧化应激并抑制Nrf2核转位；XOS以剂量依赖性方式逆转上述损伤，且该效应可被ML385阻断。SA-CS处理则显著降低细胞存活率与TEER值，下调屏障相关蛋白mRNA表达，促进细胞凋亡，升高炎症因子水平及TLR4、p-NF-κB p65蛋白表达；XOS同样以剂量依赖性方式改善上述损伤，而LPS可逆转其作用。本研究XOS通过激活Nrf2通路拮抗UVB诱导的皮肤细胞氧化损伤，通过抑制TLR4/NF-κB通路缓解SA-CS介导的炎症损伤，进而保护皮肤屏障功能。本研究为开发具有皮肤屏障保护、抗氧化及抗炎功效的化妆品原料的开发提供了实验依据与理论支撑。

关键词: 益生元, 低聚木糖, 日化产品, 皮肤屏障, 免疫功能, 氧化应激

Abstract:

To investigate the regulatory effect and molecular mechanism of xylooligosaccharides （XOS） on skin barrier immune function, we systematically evaluated two HaCaT cell models: ultraviolet B （UVB） -induced injury and Staphylococcus aureus culture supernatant （SA-CS） -induced inflammation. In the UVB injury model, HaCaT cells were irradiated with 30 mJ/cm2 UVB and then treated with low, medium and high doses of XOS （50, 100, 200 μg/mL） and an Nrf2 inhibitor （ML385） for 24 h. In the SA-CS inflammation model, cells were treated with 20% SA-CS for 24 h, with low, medium and high doses of XOS and a TLR4 agonist （LPS） added simultaneously. Each group consisted of six replicate wells. Cell viability, apoptosis rate （TUNEL assay）, mRNA levels of apoptosis-related genes （Bax, Bcl-2）, transepithelial electrical resistance （TEER） value, mRNA levels of barrier-related proteins （FLG, Claudin-1/4）, oxidative stress indicators （ROS, MDA, SOD）, proteins of the Nrf2/Keap1 pathway, inflammatory factors （IL-1β, IL-8, TNF-α, etc.） and protein levels of the TLR4/NF-κB pathway were measured. The results show that UVB irradiation significantly decreases cell viability and TEER value, downregulates mRNA expression of barrier-related proteins, promotes cell apoptosis, induces oxidative stress and inhibits Nrf2 nuclear translocation in HaCaT cells. XOS reverses these injuries in a dose-dependent manner, an effect that can be blocked by ML385. SA-CS treatment significantly reduces cell viability and TEER value, downregulates mRNA expression of barrier-related proteins, promotes cell apoptosis, and increases the levels of inflammatory factors and protein expression of TLR4 and p-NF-κB p65. XOS also ameliorates these injuries in a dose-dependent manner, while LPS reverses this effect. In summary, XOS antagonizes UVB-induced oxidative damage in skin cells by activating the Nrf2 pathway, and alleviates SA-CS-mediated inflammatory damage by inhibiting the TLR4/NF-κB pathway, thereby protecting skin barrier function. This study provides experimental evidence and theoretical support for the development of cosmetic raw materials with skin barrier protection, antioxidant and anti-inflammatory effects.

Key words: prebiotics, xylooligosaccharides （XOS）, daily chemical products, skin barrier, immune function, oxidative stress

中图分类号: 

  • TQ658