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肌肽和视黄醇通过上调透明质酸合酶2协同抑制紫外线B诱导的人角质形成细胞中前列腺素E的合成。

Carnosine and Retinol Synergistically Inhibit UVB-Induced PGE Synthesis in Human Keratinocytes through the Up-Regulation of Hyaluronan Synthase 2.

作者信息

Park In Guk, Jin Sun Hee, An Seungchan, Ki Min Won, Park Won Seok, Kim Hyoung-June, Na Yongjoo, Noh Minsoo

机构信息

Natural Products Research Institute, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.

Basic Research & Innovation Division, AmorePacific Corporation R&I Center, Yongin 17074, Republic of Korea.

出版信息

Biomol Ther (Seoul). 2024 Sep 1;32(5):635-639. doi: 10.4062/biomolther.2023.226. Epub 2024 Aug 2.

DOI:10.4062/biomolther.2023.226
PMID:39091010
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11392658/
Abstract

Skin aging results from complex interactions of intrinsic and extrinsic factors, leading to structural and biochemical changes such as wrinkles and dryness. Ultraviolet (UV) irradiation leads to the degradation of hyaluronic acid (HA) in the skin, and the with fragmented HA contributes to inflammation. This study revealed that the synergistic combination of carnosine and retinol (ROL) increases HA production in normal human epidermal keratinocytes (NHEKs) by upregulating hyaluronan synthase 2 (HAS2) gene transcription. Simultaneously, the combined treatment of carnosine and ROL significantly attenuates UVB-induced prostaglandin E (PGE) synthesis in NHEKs. A significant correlation exists between the increase of HA synthesis and the inhibition of PGE production. This study suggested that combined treatment of carnosine and ROL can improve skin aging phenotypes associated with UVB irradiation.

摘要

皮肤老化是由内在和外在因素的复杂相互作用引起的，会导致结构和生化变化，如皱纹和干燥。紫外线（UV）照射会导致皮肤中透明质酸（HA）降解，而碎片化的HA会引发炎症。本研究表明，肌肽和视黄醇（ROL）的协同组合通过上调透明质酸合酶2（HAS2）基因转录，增加正常人表皮角质形成细胞（NHEKs）中HA的生成。同时，肌肽和ROL联合处理可显著减弱UVB诱导的NHEKs中前列腺素E（PGE）的合成。HA合成增加与PGE生成抑制之间存在显著相关性。本研究提示，肌肽和ROL联合处理可改善与UVB照射相关的皮肤老化表型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be0/11392658/cc950022ccdf/bt-32-5-635-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be0/11392658/545cfe812c04/bt-32-5-635-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be0/11392658/cc950022ccdf/bt-32-5-635-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be0/11392658/545cfe812c04/bt-32-5-635-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be0/11392658/93a4e7808bd8/bt-32-5-635-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be0/11392658/604cecb1a52c/bt-32-5-635-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8be0/11392658/cc950022ccdf/bt-32-5-635-f4.jpg

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