Xu Ying, Liu Yue, Li Junxiang, Li Yao, Xu Linlin, Dong Kun, Lin Xiao, Zhang Tao
Better Way (Shanghai) Cosmetics Co. Ltd., Shanghai, China.
AGECODE R&D Center, Yangtze Delta Region Institute of Tsinghua University, Jiaxing, Zhejiang, China.
Front Med (Lausanne). 2025 Mar 28;12:1556680. doi: 10.3389/fmed.2025.1556680. eCollection 2025.
Sensitive skin is characterized by a disrupted skin barrier, making it prone to reacting to external stimuli, including UV exposure, air pollution, and cosmetic allergens. Sensitive skin tends to react with oxidative stress factors that could further lead to inflammation and subsequently result in inflammaging. However, there are almost no existing inflammaging models specifically for sensitive skin, highlighting the need to develop a method for screening anti-inflammaging ingredients and products.
An macrophage-fibroblast model was established to evaluate the anti-inflammaging effects of the ingredients. The M1 phenotype and aging-associated gene expression were assessed using qPCR to validate the inflammaging model. RNA sequencing was used to further elucidate the inflammaging mechanisms of the two validated ingredients.
A novel model of sensitive skin inflammaging was developed by applying the supernatant of the M1 macrophage culture medium to induce cellular senescence in fibroblast cells, facilitating the screening of anti-inflammaging ingredients. In this model, supramolecular bakuchiol could promote collagen COL1A1 and COL3A3 production and inhibit inflammatory factors by enhancing the transcription of anti-inflammatory genes (, and ), while extract inhibits cell senescence by reducing the transcription of MAP4K2 and the accumulation of the inflammatory factor CCL3.
敏感性皮肤的特征是皮肤屏障受损,使其易于对外界刺激产生反应,包括紫外线照射、空气污染和化妆品过敏原。敏感性皮肤往往会与氧化应激因素发生反应,这可能会进一步导致炎症,进而导致皮肤老化。然而,几乎没有专门针对敏感性皮肤的皮肤老化模型,这凸显了开发一种筛选抗皮肤老化成分和产品方法的必要性。
建立巨噬细胞-成纤维细胞模型来评估成分的抗皮肤老化作用。使用qPCR评估M1表型和衰老相关基因表达,以验证皮肤老化模型。RNA测序用于进一步阐明两种经过验证的成分的皮肤老化机制。
通过应用M1巨噬细胞培养基的上清液诱导成纤维细胞中的细胞衰老,开发了一种新的敏感性皮肤老化模型,便于筛选抗皮肤老化成分。在该模型中,超分子补骨脂酚可通过增强抗炎基因( 、 和 )的转录来促进胶原蛋白COL1A1和COL3A3的产生并抑制炎症因子,而 提取物通过减少MAP4K2的转录和炎症因子CCL3的积累来抑制细胞衰老。