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依克多因通过抑制糖皮质激素受体(GR)信号传导以及紫外线B(UVB)诱导的11β-羟基类固醇脱氢酶1(11β-HSD1)过表达来减轻可的松诱导的皮肤问题。

Ectoin attenuates cortisone-induced skin issues by suppression GR signaling and the UVB-induced overexpression of 11β-HSD1.

作者信息

Xu Dailin, Wu Yue

机构信息

In Vitro Research Department, Bloomage Biotechnology Corporation Limited, Shanghai, China.

出版信息

J Cosmet Dermatol. 2024 Dec;23(12):4303-4314. doi: 10.1111/jocd.16516. Epub 2024 Sep 2.

DOI:10.1111/jocd.16516
PMID:39222375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11626367/
Abstract

BACKGROUND

Accelerated pace of modern work and lifestyles subject individuals to various external and psychological stressors, which, in turn, can trigger additional stress through visible signs of fatigue, hair loss, and obesity. As the primary stress hormone affecting skin health, cortisol connects to the glucocorticoid receptor (GR) to aggravate skin issues induced by stress. This activation depends on the expression of 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) in skin cells, which locally converts cortisone-produced by the central and peripheral hypothalamic-pituitary-adrenal axis-into its active form.

METHODS

Our study delves deeper into stress's adverse effects on the skin, including the disruption of keratinocyte structural proteins, the loss of basement membrane proteins, and the degradation of collagen.

RESULTS

Remarkably, we discovered that Ectoin, an amino acid derivative obtained from halophilic bacteria, is capable of mitigating the inhibitory impacts of cortisone on the expression of cutaneous functional proteins, including involucrin, loricrin, laminin-5, and claudin-1. Moreover, Ectoin reduces the suppressive effect of stress on collagen and hyaluronic acid synthesis by impeding GR signal transduction. Additionally, Ectoin counterbalances the UVB-induced overexpression of 11β-HSD1, thereby diminishing the concentration of endogenous glucocorticoids.

CONCLUSION

Our findings illuminate the significant potential of Ectoin as a preventative agent against stress-induced skin maladies.

摘要

背景

现代工作和生活节奏的加快使个体面临各种外部和心理压力源,这些压力源又会通过疲劳、脱发和肥胖等明显迹象引发额外的压力。作为影响皮肤健康的主要应激激素,皮质醇与糖皮质激素受体(GR)结合,加重压力引起的皮肤问题。这种激活取决于皮肤细胞中11β-羟基类固醇脱氢酶1(11β-HSD1)的表达,该酶可将中枢和外周下丘脑-垂体-肾上腺轴产生的可的松局部转化为其活性形式。

方法

我们的研究更深入地探讨了压力对皮肤的不良影响,包括角质形成细胞结构蛋白的破坏、基底膜蛋白的丢失和胶原蛋白的降解。

结果

值得注意的是,我们发现从嗜盐细菌中获得的氨基酸衍生物依克多因能够减轻可的松对皮肤功能蛋白表达的抑制作用,这些蛋白包括兜甲蛋白、loricrin、层粘连蛋白-5和闭合蛋白-1。此外,依克多因通过阻碍GR信号转导,降低了压力对胶原蛋白和透明质酸合成的抑制作用。此外,依克多因还能抵消紫外线B诱导的11β-HSD1过表达,从而降低内源性糖皮质激素的浓度。

结论

我们的研究结果揭示了依克多因作为预防压力引起的皮肤疾病的药物具有巨大潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/14fd4671a5d4/JOCD-23--g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/34004ab75532/JOCD-23--g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/09231edbd541/JOCD-23--g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/21be42e658b9/JOCD-23--g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/34d8827bee46/JOCD-23--g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/b9f3fbbaddfe/JOCD-23--g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/6f677e790f74/JOCD-23--g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/14fd4671a5d4/JOCD-23--g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/34004ab75532/JOCD-23--g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/09231edbd541/JOCD-23--g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/21be42e658b9/JOCD-23--g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/34d8827bee46/JOCD-23--g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/b9f3fbbaddfe/JOCD-23--g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/6f677e790f74/JOCD-23--g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b88e/11626367/14fd4671a5d4/JOCD-23--g005.jpg

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