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具有抗炎和抗氧化作用的琥珀酰壳寡糖可保护人表皮细胞和小鼠皮肤免受紫外线B诱导的光损伤。

Anti-inflammatory and antioxidant succinyl-chitosan oligosaccharide protects human epidermal cell and mouse skin against ultraviolet B-induced photodamage.

作者信息

Lv Xiansen, Han Zi, Huo Huilin, Liu Xiaofei, Zhang Jinpeng, Chi Jinhua, Han Baoqin, Jiang Zhiwen

机构信息

Laboratory of Biochemistry and Biomedical Materials, College of Marine Life Sciences, Ocean University of China, Qingdao 266003, PR China.

Laboratory of Biochemistry and Biomedical Materials, College of Marine Life Sciences, Ocean University of China, Qingdao 266003, PR China.

出版信息

Carbohydr Polym. 2025 Mar 1;351:123102. doi: 10.1016/j.carbpol.2024.123102. Epub 2024 Dec 3.

DOI:10.1016/j.carbpol.2024.123102
PMID:39779016
Abstract

Ultraviolet B (UVB) irradiation from sunlight is one of the primary environmental factors that causes photodamage to the skin. The aim of this study was to prepare succinyl-chitosan oligosaccharide (SU-COS) and evaluate its protective effects and related molecular mechanisms against UVB-induced photodamage for the first time. SU-COS (substitution degree: 69.26 %, molecular weight: 6400 Da) was shown to have excellent biocompatibility and to effectively promote the migration of human epidermal HaCaT cells. UVB irradiation was used to develop photodamage models in HaCaT cells and murine skin. In vitro, treatment with SU-COS significantly increased the cell survival ratio by >11 % while concurrently reducing reactive oxygen species formation, preserving normal cytoskeletal morphology, stabilizing the cell cycle, and decreasing the apoptosis ratio. The SU-COS intervention also demonstrated a reparative effect on UVB-damaged mouse skin by reducing skin erythema and water loss, relieving crusting, and maintaining the epidermis thickness of the skin and the stability of collagen fibers. The observed changes in both in vitro and in vivo results were accompanied by significant modulation of gene and protein expression associated with the cellular cycle, collagen synthesis, extracellular matrix degradation, antioxidant defense, and inflammation. Overall, SU-COS holds immense promise for applications in repairing photodamage.

摘要

阳光中的紫外线B(UVB)辐射是导致皮肤光损伤的主要环境因素之一。本研究的目的是首次制备琥珀酰壳寡糖(SU-COS),并评估其对UVB诱导的光损伤的保护作用及相关分子机制。结果表明,SU-COS(取代度:69.26%,分子量:6400 Da)具有优异的生物相容性,并能有效促进人表皮HaCaT细胞的迁移。采用UVB辐射建立HaCaT细胞和小鼠皮肤的光损伤模型。在体外,SU-COS处理显著提高了细胞存活率超过11%,同时减少了活性氧的生成,保持了正常的细胞骨架形态,稳定了细胞周期,并降低了凋亡率。SU-COS干预还通过减少皮肤红斑和水分流失、缓解结痂、维持皮肤表皮厚度和胶原纤维稳定性,对UVB损伤的小鼠皮肤表现出修复作用。体外和体内实验结果观察到的变化均伴随着与细胞周期、胶原合成、细胞外基质降解、抗氧化防御和炎症相关的基因和蛋白质表达的显著调节。总体而言,SU-COS在修复光损伤方面具有巨大的应用前景。

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