<br>尿囊素、红没药醇、D-泛醇和甘草酸二钾的组合可减轻 UVB 诱导的角质形成细胞的 PGE2 合成,International Journal of Cosmetic Science

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尿囊素、红没药醇、D-泛醇和甘草酸二钾的组合可减轻 UVB 诱导的角质形成细胞的 PGE2 合成
International Journal of Cosmetic Science ( IF 2.7 ) Pub Date : 2024-03-04 , DOI: 10.1111/ics.12951
Chelsea Tan ₁ , Ke Peng ₂ , TianYong Lim ₁ , Jiaxin Liu ₃ , Yang Ye ₂ , Linda Lim ₁ , Pei Gao ₃ , John E Oblong ₄ , TzeHau Lam ₁

Affiliation

目的红斑是由多种内源性和外源性因素引起的常见皮肤反应，以皮肤发红为特征。这种反应通常是皮肤内潜在炎症机制激活的结果。本研究的目的是探讨尿囊素、红没药醇、D-泛醇和甘草酸二钾 (AB5D) 等护肤成分组合在调节与红斑相关的炎症因子方面的潜在益处。此外，该研究旨在阐明这些成分发挥联合作用以减轻红斑相关炎症的机制。方法将人表皮角质形成细胞暴露于 UVB，随后用 AB5D 进行处理。进行转录组学分析来分析 AB5D 治疗对角质形成细胞的剂量反应效应。在培养基上对炎症介质（包括 PGE2、IL-1α、IL-6、IL-8、IL-1RA 和 TNFα）进行定量。此外，还进行了氧自由基吸收能力 (ORAC) 测定，以评估单个成分和 AB5D 组合的总抗氧化能力。为了评估 AB5D 对 hTERT 角质形成细胞中 UVB 诱导的氧化应激的体外抗氧化作用，通过活细胞成像对线粒体超氧化物进行实时定量。结果将 AB5D 应用于 UVB 暴露的角质形成细胞，下调了与炎症相关的基因组。反应，突出了 AB5D 的抗炎特性。具体来说，AB5D 有效减少 PGE2 的产生，从而导致炎症细胞因子的下调。此外，我们的研究结果表明，AB5D 具有抗氧化能力，既可作为抗氧化剂，又可作为抗氧化酶表达的调节剂，以抵消细胞氧化应激的有害影响。结论我们证明，AB5D 可以减少 UVB 诱导的 PGE2、IL-1α、IL ‐6、IL-8、IL-1RA 和 TNFα 以及线粒体超氧化物。这些发现表明 AB5D 可能通过 PGE2 调节炎症和抗氧化机制来减轻红斑。

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The combination of allantoin, bisabolol, D‐panthenol and dipotassium glycyrrhizinate mitigates UVB‐induced PGE2 synthesis by keratinocytes

ObjectiveErythema, characterized by the redness of the skin, is a common skin reaction triggered by various endogenous and exogenous factors. This response is often a result of the activation of underlying inflammatory mechanisms within the skin. The objective of this study is to investigate the potential benefits of applying a combination of skincare ingredients, namely allantoin, bisabolol, D‐panthenol and dipotassium glycyrrhizinate (AB5D), in the modulation of inflammatory factors associated with erythema. Additionally, the study aims to elucidate the mechanisms by which these ingredients exert their combined actions to alleviate erythema‐associated inflammation.MethodsHuman epidermal keratinocytes were exposed to UVB and subsequently treated with AB5D. Transcriptomics profiling was performed to analyse the dose–response effect of AB5D treatment on keratinocytes. The quantitation of inflammatory mediators, including PGE2, IL‐1α, IL‐6, IL‐8, IL‐1RA and TNFα, was performed on cultured media. Additionally, the oxygen radical absorbance capacity (ORAC) assay was carried out to evaluate the total antioxidant capacity of both individual ingredients and the AB5D combination. To assess the in‐vitro antioxidant effects of AB5D against UVB‐induced oxidative stress in hTERT keratinocytes, real‐time quantitation of mitochondrial superoxide was measured through live‐cell imaging.ResultsThe application of AB5D to UVB‐exposed keratinocytes downregulated gene sets associated with inflammatory responses, highlighting the anti‐inflammatory properties of AB5D. Specifically, AB5D effectively reduced the production of PGE2, leading to the downregulation of inflammatory cytokines. Moreover, our findings indicate that AB5D exhibits antioxidative capabilities, functioning as both an antioxidant agent and a regulator of antioxidant enzyme expression to counteract the detrimental effects of cellular oxidative stress.ConclusionWe demonstrated that AB5D can reduce UVB‐induced PGE2, IL‐1α, IL‐6, IL‐8, IL‐1RA and TNFα as well as mitochondrial superoxide. These findings suggest that AB5D may alleviate erythema by modulating inflammation via PGE2 and through antioxidation mechanisms.

更新日期：2024-03-04

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