泛醇多通路协同对紫外线暴露皮肤真/表皮损伤的保护作用  

Panthenol Protects Against Epidermal and Dermal Skin Damage from Ultraviolet Exposure Through Multiple Pathways

作　　者：王静一 黄云霞 陶侃 钟涛 黄虎 常怀龙 WANG Jingyi;HUANG Yunxia;TAO Kan;ZHONG Tao;HUANG Hu;CHANG Huailong(Global R&D Center,Shanghai Chicmax Cosmetic Co.,Ltd.,Shanghai 200065,China)

机构地区：[1]上海上美化妆品股份有限公司全球研发中心,上海200065

出　　处：《皮肤科学通报》2024年第6期621-628,共8页Dermatology Bulletin

摘　　要：目的探究泛醇对紫外线暴露皮肤损伤的保护作用及作用机制。方法利用转录组学技术研究了泛醇对UVB刺激表皮皮肤模型的影响,并对差异表达基因进行了富集和聚类分析。采用紫外线诱导角质形成细胞、成纤维细胞和表皮皮肤模型分析了泛醇对细胞存活情况、炎症因子分泌量、抗氧化酶基因表达水平以及活性氧自由基含量的影响。结果在表皮层,泛醇可以增加UVB刺激下角质形成细胞的存活数量,抑制炎症因子IL-1α和炎症介质PGE2的分泌,降低3D表皮皮肤模型中ROS含量。在真皮层,泛醇可以提升成纤维细胞中抗氧化酶的表达水平,降低UVA处理后细胞中ROS含量。结论泛醇对皮肤紫外损伤的保护作用可能与抑制细胞凋亡、舒缓细胞炎症、减轻氧化应激有关。Objective To investigate the protective effect of panthenol on skin UV damage and explore the potential pathways.Methods The transcriptomic analysis of the UVB-stimulated epidermal skin models was conducted,and the enrichment and clustering analysis were performed on differentially expressed genes.We also explored the effects of panthenol on UVR-stimulated keratinocytes,fibroblasts,and epidermal models by evaluating cell viability rates,contents of inflammatory cytokines and chemokines,gene expression levels of the antioxidant enzymes,and contents of reactive oxygen species.Results In the epidermis,panthenol increased the viability rate of keratinocytes under UVB stimulation,inhibited the secretion of the inflammatory cytokine IL-1αand the inflammatory chemokine PGE2,and reduced the ROS content in the 3D epidermal skin model.In the dermis,panthenol enhance the expression levels of antioxidant enzymes in fibroblasts and reduced cell ROS content after UVA treatment.Conclusion The protective effect of panthenol on skin UV damage may be related to inhibiting cell apoptosis,soothing cell inflammation,and alleviating oxidative stress.

关 键 词：泛醇 紫外损伤 炎症反应 氧化应激 皮肤 

分 类 号：R758[医药卫生—皮肤病学与性病学]