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普兰奇通过控制活性氧/AKT信号通路改善紫外线B照射的NIH-3T3细胞和SKH-1无毛小鼠的光老化。

Planch Ameliorates Photoaging in UVB-Irradiated NIH-3T3 Cells and SKH-1 Hairless Mice by Controlling the Reactive Oxygen Species/AKT Pathway.

作者信息

Jung Jong-Min, Kim Seo-Young, Kwon Oh-Yun, Lee Seung-Ho

机构信息

Department of Nano-Bioengineering, Incheon National University, 119 Academy-ro, Incheon 22012, Republic of Korea.

出版信息

Antioxidants (Basel). 2024 Sep 6;13(9):1091. doi: 10.3390/antiox13091091.

Abstract

In this study, we evaluated the antiphotoaging properties of Planch (ACP) and the molecular mechanisms underlying its ability to prevent UVB-mediated photoaging. Administration of the ethanolic extract of ACP (EEACP) to the dorsal area of hairless mice effectively ameliorated UVB-mediated wrinkle formation, epidermal thickening, and loss of lipid droplets in the epidermis. Additionally, the UVB-induced loss of collagen content in the epidermis was significantly attenuated in mouse skin treated with EEACP. The expression of procollagen type 1 and metalloproteinase-1a, which are related to collagen content in the epidermis, was restored by EEACP treatment in UVB-irradiated mice and NIH-3T3 mouse skin fibroblast cells. Interestingly, EEACP effectively ameliorated UVB-induced reactive oxygen species overproduction. Furthermore, the activation/phosphorylation of AKT, rather than mitogen-activated protein kinases, has been identified as a major target of EEACP in preventing UVB-mediated photoaging. Additionally, N-(1 deoxy-1-fructosyl) valine and phenethylamine glucuronide were identified as analytical indicators of EEACP using high-performance liquid chromatography/mass spectrometry. These results suggest that EEACP can be developed as a functional natural agent capable of preventing photoaging by attenuating UVB-induced activation of the reactive oxygen species/AKT pathway.

摘要

在本研究中,我们评估了光果甘草提取物(ACP)的抗光老化特性及其预防紫外线B(UVB)介导的光老化能力的潜在分子机制。将ACP乙醇提取物(EEACP)施用于无毛小鼠背部区域,可有效改善UVB介导的皱纹形成、表皮增厚以及表皮脂质小滴的丢失。此外,在经EEACP处理的小鼠皮肤中,UVB诱导的表皮胶原蛋白含量的减少显著减轻。在UVB照射的小鼠和NIH-3T3小鼠皮肤成纤维细胞中,通过EEACP处理可恢复与表皮胶原蛋白含量相关的I型前胶原蛋白和金属蛋白酶-1a的表达。有趣的是,EEACP可有效改善UVB诱导的活性氧过量产生。此外,已确定AKT的激活/磷酸化而非丝裂原活化蛋白激酶是EEACP预防UVB介导的光老化的主要靶点。此外,使用高效液相色谱/质谱法将N-(1-脱氧-1-果糖基)缬氨酸和苯乙胺葡糖醛酸苷鉴定为EEACP的分析指标。这些结果表明,EEACP可开发成为一种功能性天然制剂,通过减弱UVB诱导的活性氧/AKT途径的激活来预防光老化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3448/11428346/98ad0bdeeb58/antioxidants-13-01091-g001.jpg

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