通过抑制人类角质细胞和无毛小鼠体内的丝裂原活化蛋白激酶/激活蛋白1/基质金属蛋白酶1通路,柿叶提取物可减轻紫外线B诱导的光老化现象

Ji-Ae Hong , Hae-ju Ko , Kyo-Nyeo Oh , Moonjong Kim , Jung-Soon Mo , Chul Yung Choi , Ki-Man Kim , Donghyuk Bae
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引用次数: 0

摘要

紫外线(UV)照射被认为是皮肤光老化的主要诱因,其特点是基质金属蛋白酶(MMPs)和活性氧(ROS)的过度产生,以及细胞外基质(ECM)蛋白质的加速分解,最终导致皱纹的产生。柿树(PS)提取物的抗氧化特性及其对皮肤健康的重要性已得到公认。然而,目前还很少有研究调查 PS 在保护皮肤免受光老化影响方面的潜力。本研究旨在利用永生的人类角质细胞(HaCaT)和无毛小鼠,评估 PS 提取物在防止光老化方面的功效,并阐明其中的分子机制。经鉴定,PS 的主要生物活性成分为对香豆酸、异槲皮苷、槲皮素-3-O-葡萄糖醛酸苷和槲皮素。PS 的水提取物具有减轻 UVB 诱导的细胞损伤和减少 HaCaT 细胞中 ROS 生成的能力。此外,用 PS 处理可有效减轻 UVB 暴露引起的基质金属蛋白酶-1(MMP-1)表达上调和胶原降解。PS 抵抗光老化的特性与其抑制 UVB 诱导的丝裂原活化蛋白激酶(MAPK)磷酸化和抑制随后激活的激活蛋白 1(AP-1)信号通路的能力有关。此外,在暴露于紫外线辐射下的无毛小鼠身上涂抹 PS 能明显缓解皮肤皱纹的形成,减少表皮增厚,并减轻胶原降解。值得注意的是,PS 处理可下调小鼠皮肤组织中由 UVB 激活的 MAPK/AP-1/MMP-1 通路。这些研究结果表明,PS 有可能成为一种治疗光老化的药物,在化妆品和医药应用方面都大有可为。
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Persicaria senticosa extract mitigates ultraviolet B-induced photoaging by suppressing the mitogen-activated protein kinase/activator protein 1/matrix metalloproteinase 1 pathway in human keratinocytes and hairless mice

Ultraviolet (UV) irradiation has been identified as a key trigger for skin photoaging, characterized by the overproduction of matrix metalloproteinases (MMPs) and reactive oxygen species (ROS), along with the accelerated decomposition of extracellular matrix (ECM) proteins, ultimately contributing to the development of wrinkles. Persicaria senticosa (PS) extracts are recognized for their antioxidative properties and their importance in skin health. Nevertheless, there is a paucity of studies investigating the potential of PS in protecting the skin against photoaging. The present study aimed to assess the effectiveness of PS extracts in preventing photoaging and elucidating the molecular mechanisms involved in using immortalized human keratinocytes (HaCaT) and hairless mice. The major bioactive constituents of PS were identified as p-coumaric acid, isoquercitrin, quercetin-3-O-glucuronide, and quercetin. Aqueous extracts of PS exhibited the ability to mitigate UVB-induced cellular damage and diminished ROS generation in HaCaT cells. Moreover, treatment with PS effectively attenuated the upregulated expression of matrix metalloproteinase-1 (MMP-1) and collagen degradation induced by UVB exposure. The property of PS to counteract photoaging was related to its capacity to inhibit the UVB-induced phosphorylation of mitogen-activated protein kinase (MAPK) and suppress the subsequent activation of activator protein 1 (AP-1) signaling pathways. Moreover, in hairless mice exposed to UVB radiation, the application of PS significantly alleviated the development of skin wrinkles, diminished epidermal thickening, and mitigated collagen degradation. Notably, PS treatment resulted in the downregulation of the UVB-activated MAPK/AP-1/MMP-1 pathway in mouse skin tissues. These findings suggest that PS has the potential to serve as a therapeutic agent for treating photoaging, holding promises in both cosmeceutical and pharmaceutical applications.

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