Jeju Research Center for Natural Medicine, Jeju National University, Jeju 63243, Republic of Korea; Department of Biochemistry, College of Medicine, Jeju National University, Jeju 63243, Republic of Korea.
Department of Biochemistry, College of Medicine, Jeju National University, Jeju 63243, Republic of Korea.
Toxicol In Vitro. 2024 Aug;99:105870. doi: 10.1016/j.tiv.2024.105870. Epub 2024 Jun 6.
Particulate matter 2.5 (PM) causes skin aging, inflammation, and impaired skin homeostasis. Hyperoside, a flavanol glycoside, has been proposed to reduce the risk of diseases caused by oxidative stress. This study evaluated the cytoprotective potential of hyperoside against PM-induced skin cell damage. Cultured human HaCaT keratinocytes were pretreated with hyperoside and treated with PM. Initially, the cytoprotective and antioxidant ability of hyperoside against PM was evaluated. Western blotting was further employed to investigate endoplasmic reticulum (ER) stress and cellular senescence and for evaluation of cell cycle regulation-related proteins. Hyperoside inhibited PM-mediated ER stress as well as mitochondrial damage. Colony formation assessment confirmed that PM-impaired cell proliferation was restored by hyperoside. Moreover, hyperoside reduced the activation of PM-induced ER stress-related proteins, such as protein kinase R-like ER kinase, cleaved activating transcription factor 6, and inositol-requiring enzyme 1. Hyperoside promoted cell cycle progression in the G/G phase by upregulating the PM-impaired cell cycle regulatory proteins. Hyperoside significantly reduced the expression of PM-induced senescence-associated β-galactosidase and matrix metalloproteinases (MMPs), such as MMP-1 and MMP-9. Overall, hyperoside ameliorated PM-impaired cell proliferation, ER stress, and cellular senescence, offering potential therapeutic implications for mitigating the adverse effects of environmental pollutants on skin health.
细颗粒物 2.5 (PM) 可导致皮肤衰老、炎症和皮肤内稳态受损。山奈酚-3-O-芸香糖苷，一种黄烷醇糖苷，被提议可降低由氧化应激引起的疾病的风险。本研究评估了山奈酚-3-O-芸香糖苷对 PM 诱导的皮肤细胞损伤的细胞保护潜力。培养的人 HaCaT 角质形成细胞用山奈酚-3-O-芸香糖苷预处理并用 PM 处理。首先，评估了山奈酚-3-O-芸香糖苷对 PM 的细胞保护和抗氧化能力。进一步采用 Western blot 分析来研究内质网 (ER) 应激和细胞衰老，并评估细胞周期调控相关蛋白。山奈酚-3-O-芸香糖苷抑制 PM 介导的 ER 应激和线粒体损伤。集落形成评估证实，山奈酚-3-O-芸香糖苷恢复了 PM 损害的细胞增殖。此外，山奈酚-3-O-芸香糖苷降低了 PM 诱导的 ER 应激相关蛋白的激活，如蛋白激酶 R 样内质网激酶、切割激活转录因子 6 和肌醇需求酶 1。山奈酚-3-O-芸香糖苷通过上调 PM 损害的细胞周期调节蛋白促进细胞周期在 G/G 期的进展。山奈酚-3-O-芸香糖苷显著降低了 PM 诱导的衰老相关β-半乳糖苷酶和基质金属蛋白酶 (MMPs)，如 MMP-1 和 MMP-9 的表达。总的来说，山奈酚-3-O-芸香糖苷改善了 PM 损害的细胞增殖、ER 应激和细胞衰老，为减轻环境污染物对皮肤健康的不利影响提供了潜在的治疗意义。
