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Dieckol an Algae-Derived Phenolic Compound Suppresses UVB-Induced Skin Damage in Human Dermal Fibroblasts and Its Underlying Mechanisms

机译:Dieckol一种藻类酚类化合物抑制了人类皮肤成纤维细胞的UVB诱导的皮肤损伤及其潜在的机制

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摘要

Ultraviolet (UV) irradiation is considered to be the primary environmental factor that causes skin damage. In the present study, we investigated the protective effect of dieckol (DK), a compound isolated from the brown seaweed Ecklonia cava, against UVB-induced skin damage in human dermal fibroblasts (HDF cells). The results indicated that DK effectively inhibited the activity of collagenase. DK remarkably reduced the intracellular reactive oxygen species level and improved the viability of UVB-irradiated HDF cells. Besides, DK significantly and dose-dependently improved collagen synthesis and inhibited intracellular collagenase activity in UVB-irradiated HDF cells. In addition, DK markedly reduced the expression of proinflammatory cytokines and matrix metalloproteinases. Further analyses revealed that these processes were mediated through the regulation of nuclear factor kappa B, activator protein 1, and mitogen-activated protein kinase signaling pathways in the UVB-irradiated HDF cells. In conclusion, these results indicate that DK possesses strong in vitro photoprotective effects and therefore has the potential to be used as an ingredient in the cosmeceutical industry.
机译:紫外线(UV)辐射被认为是引起皮肤损伤的主要环境因素。在本研究中,我们研究了Dieckol(DK)的保护作用,从棕色海藻Ecklonia cava中分离的化合物,抵抗UVB诱导的人类皮肤成纤维细胞(HDF细胞)的皮肤损伤。结果表明,DK有效地抑制了胶原酶的活性。 DK显着降低细胞内反应性氧物质水平,并改善了UVB辐照的HDF细胞的活力。此外,DK显着和剂量依赖性改善胶原合成并抑制UVB辐照的HDF细胞中的细胞内胶原酶活性。另外,DK显着降低了促炎细胞因子和基质金属蛋白酶的表达。进一步的分析表明,通过调节核因子Kappa B,活化剂蛋白1和丝裂剂活化的蛋白激酶信号传导途径在UVB辐照的HDF细胞中介导这些方法。总之,这些结果表明DK具有强大的体外光保护作用,因此有可能用作化妆品行业中的成分。

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