Human Keratinocyte UVB-Protective Effects of a Low Molecular Weight Fucoidan from Sargassum horneri Purified by Step Gradient Ethanol Precipitation
Human Keratinocyte UVB-Protective Effects of a Low Molecular Weight Fucoidan from Sargassum horneri Purified by Step Gradient Ethanol Precipitation
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DOI：
10.3390/antiox9040340
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发表时间：
2020-04-01
期刊：
影响因子：
7
通讯作者：
Ahn, Ginnae
中科院分区：
文献类型：
--
作者：
Fernando, Ilekuttige Priyan Shanura;Dias, Mawalle Kankanamge Hasitha Madhawa;Ahn, Ginnae
紫外线B （UVB）辐射引起的氧化性皮肤细胞损伤是光老化的主要原因。本研究以马尾藻为原料，采用纤维素酶辅助提取，再经乙醇梯度分步沉淀，得到低分子量岩藻聚糖（SHC4）。研究了SHC4对人角化细胞抗uvb诱导的氧化应激的保护作用。通过傅里叶红外光谱（FTIR）、H-1核磁共振（NMR）、琼脂糖凝胶分子量分析和单糖组成分析对纯化的岩藻糖聚糖进行了表征。SHC4的平均分子量为60 kDa，聚焦37.43%，硫酸盐含量28.01 +/- 0.50%。该结构主要由α - l - fucp -(1 -> 4)连接聚焦单元组成。SHC4治疗剂量依赖性地降低了UVB暴露的HaCaT角质形成细胞的细胞内活性氧（ROS）水平，并增加了细胞活力。此外，SHC4剂量依赖性地抑制uvb诱导的凋亡小体形成、亚g(1)细胞积累和DNA损伤。细胞凋亡的抑制是通过线粒体介导的途径介导的，重建了线粒体膜电位的丧失。SHC4通过核因子红细胞2相关因子2 (Nrf2)/血红素加氧酶-1 （HO-1）信号通路增强细胞内抗氧化防御，促进了UVB的保护作用。进一步的研究可能会促进SHC4作为化妆品和营养化妆品的活性成分的使用。
Ultraviolet B (UVB) radiation-induced oxidative skin cell damage is a major cause of photoaging. In the present study, a low molecular weight fucoidan fraction (SHC4) was obtained from Sargassum horneri by Celluclast-assisted extraction, followed by step gradient ethanol precipitation. The protective effect of SHC4 was investigated in human keratinocytes against UVB-induced oxidative stress. The purified fucoidan was characterized by Fourier-transform infrared spectroscopy (FTIR), H-1 nuclear magnetic resonance (NMR), agarose gel-based molecular weight analysis and monosaccharide composition analysis. SHC4 had a mean molecular weight of 60 kDa, with 37.43% fucose and 28.01 +/- 0.50% sulfate content. The structure was mainly composed of alpha-L-Fucp-(1 -> 4) linked fucose units. SHC4 treatment dose-dependently reduced intracellular reactive oxygen species (ROS) levels and increased the cell viability of UVB exposed HaCaT keratinocytes. Moreover, SHC4 dose-dependently inhibited UVB-induced apoptotic body formation, sub-G(1) accumulation of cells and DNA damage. Inhibition of apoptosis was mediated via the mitochondria-mediated pathway, re-establishing the loss of mitochondrial membrane potential. The UVB protective effect of SHC4 was facilitated by enhancing intracellular antioxidant defense via nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling. Further studies may promote the use of SHC4 as an active ingredient in cosmetics and nutricosmetics.