首页|期刊导航|日用化学工业(中英文)|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

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OA

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

中文摘要英文摘要

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.

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.

张瑞敏;张磊;何亚飞;范丽敏

濮阳医学高等专科学校,河南 濮阳 457000北京中日友好医院,北京 100029濮阳医学高等专科学校,河南 濮阳 457000濮阳医学高等专科学校,河南 濮阳 457000

化学化工

益生元低聚木糖日化产品皮肤屏障免疫功能氧化应激

prebioticsxylooligosaccharides(XOS)daily chemical productsskin barrierimmune functionoxidative stress

《日用化学工业(中英文)》 2026 (5)

603-613,11

2025年度河南省高校人文社会科学研究一般项目(2025-ZZJH-128)

10.3969/j.issn.2097-2806.2026.05.007

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