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嗜热栖热菌与依克多因共发酵产物对皮肤光损伤的修复作用

The Reduction of Skin Photodamage by the Ectoine-Thermus thermophilus Cofermentation Products.

作者信息

Wang Yiyu, Liang Jiayi, Zhang Pengkun, Yan Guihui, Jiang Hui, Wang Meijing

机构信息

Hangzhou Sanshi Cosmetics Co. Ltd, Hangzhou, China.

College of Life Sciences, Zhejiang University, Hangzhou, China.

出版信息

J Cosmet Dermatol. 2025 Jul;24(7):e70298. doi: 10.1111/jocd.70298.

DOI:10.1111/jocd.70298
PMID:40552640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12186289/
Abstract

BACKGROUND

Prolonged exposure to UVB (280-320 nm) can lead to skin oxidative damage, inflammatory response, and skin cancer. Many active ingredients in the fermentation products of Thermus thermophilus have been shown to play important roles in antioxidant and anti-UVB photodamage, such as superoxide dismutase (SOD) and photolyase. Ectoine, as one of the most prevalent compatible solutes in halophilic bacteria, can protect cells, proteins, cell membranes, and nucleic acids from external extreme environments such as high temperature, freezing, irradiation, and drying. It has been applied in the industries of fine chemicals, biomedicine, and biomanufacturing worldwide.

AIMS

In this study, we evaluated the antioxidant activities and anti-UVB photodamage activities of Ectoine-T. thermophilus cofermentation products (D-Ectoine).

METHODS

The comparison between D-Ectoine and Ectoine was analyzed with hydroxyl radical (OH·) scavenging assay, superoxide anion (O·) assay, total antioxidant capacity (T-AOC) assay, and 1,1-diphenyl-2-picrylhydrazyl radical (DPPH) scavenging assay. We evaluated the antioxidant ability of D-Ectoine by detecting malondialdehyde (MDA) levels: the activity of SOD, catalase (CAT), and glutathione peroxidase (GSH-PX) in human skin fibroblast (HSF) cells. Inflammatory response was measured with lipopolysaccharides (LPS) induced expression of interleukin 6 (IL-6) and interleukin 8 (IL-8). We evaluated the protective ability of D-Ectoine against UVB-induced damage by detecting the content of collagen type I (Col I) and extracellular matrix metalloproteinase (MMP-1) in the cells, and the number of cell survival, erythroid 2-related factor 2 (Nrf2) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) expression in 3D skin model.

RESULTS

The results showed that D-Ectione could promote the GSH-PX activity in HSF cells with stronger T-AOC and DPPH scavenging capacity, reduce the expression of LPS-induced inflammatory factors IL-6 and IL-8, increase Col I expression both with and without UVB and inhibit expression of MMP-1 after UVB irradiation. In the 3D skin model, D-Ectione could increase the number of cell survival and Nrf2 expression, and decrease 8-OHdG expression after UVB irradiation.

CONCLUSIONS

These results demonstrated that D-Ectione has protective effects against UVB-induced skin photodamage and may contribute to the development of cosmetic products with anti-UVB.

摘要

背景

长期暴露于中波紫外线(280 - 320纳米)会导致皮肤氧化损伤、炎症反应和皮肤癌。嗜热栖热菌发酵产物中的许多活性成分已被证明在抗氧化和抗中波紫外线光损伤方面发挥重要作用,如超氧化物歧化酶(SOD)和光解酶。依克多因作为嗜盐细菌中最普遍的相容性溶质之一,可以保护细胞、蛋白质、细胞膜和核酸免受高温、冷冻、辐射和干燥等外部极端环境的影响。它已在全球精细化工、生物医药和生物制造等行业得到应用。

目的

在本研究中,我们评估了依克多因 - 嗜热栖热菌共发酵产物(D - 依克多因)的抗氧化活性和抗中波紫外线光损伤活性。

方法

通过羟自由基(OH·)清除试验、超氧阴离子(O·)试验、总抗氧化能力(T - AOC)试验和1,1 - 二苯基 - 2 - 苦基肼自由基(DPPH)清除试验分析D - 依克多因和依克多因之间的差异。我们通过检测丙二醛(MDA)水平来评估D - 依克多因的抗氧化能力:检测人皮肤成纤维细胞(HSF)中SOD、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH - PX)的活性。用脂多糖(LPS)诱导的白细胞介素6(IL - 6)和白细胞介素8(IL - 8)表达来测量炎症反应。我们通过检测细胞中I型胶原蛋白(Col I)和细胞外基质金属蛋白酶(MMP - 1)的含量,以及3D皮肤模型中的细胞存活数量、红细胞2相关因子2(Nrf2)和8 - 羟基 - 2'-脱氧鸟苷(8 - OHdG)表达来评估D - 依克多因对中波紫外线诱导损伤的保护能力。

结果

结果表明,D - 依克多因可以促进HSF细胞中GSH - PX活性,具有更强的T - AOC和DPPH清除能力,降低LPS诱导的炎症因子IL - 6和IL - 8的表达,在有或没有中波紫外线照射的情况下均增加Col I表达,并抑制中波紫外线照射后MMP - 1的表达。在3D皮肤模型中,D - 依克多因可以增加细胞存活数量和Nrf2表达,并降低中波紫外线照射后8 - OHdG的表达。

结论

这些结果表明,D - 依克多因对中波紫外线诱导的皮肤光损伤具有保护作用,可能有助于开发具有抗中波紫外线功能的化妆品。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/97252c735b0a/JOCD-24-e70298-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/7338e771c64f/JOCD-24-e70298-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/ef845db18627/JOCD-24-e70298-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/eb8b7d92b186/JOCD-24-e70298-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/60918985464e/JOCD-24-e70298-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/c0354a00d35c/JOCD-24-e70298-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/6b8aa47cf518/JOCD-24-e70298-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/69428f9e7363/JOCD-24-e70298-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/3cd565b259fb/JOCD-24-e70298-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/97252c735b0a/JOCD-24-e70298-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/7338e771c64f/JOCD-24-e70298-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/ef845db18627/JOCD-24-e70298-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/eb8b7d92b186/JOCD-24-e70298-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/60918985464e/JOCD-24-e70298-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/c0354a00d35c/JOCD-24-e70298-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/6b8aa47cf518/JOCD-24-e70298-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/69428f9e7363/JOCD-24-e70298-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/3cd565b259fb/JOCD-24-e70298-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98f5/12186289/97252c735b0a/JOCD-24-e70298-g007.jpg

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