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淫羊藿苷和淫羊藿次苷通过激活 Nrf2/ARE 并减少 AP-1 和 NF-κB 信号通路来恢复 UVB 诱导的光老化:UVB 照射人角质形成细胞的比较研究。

Icariin and icaritin recover UVB-induced photoaging by stimulating Nrf2/ARE and reducing AP-1 and NF-κB signaling pathways: a comparative study on UVB-irradiated human keratinocytes.

机构信息

College of Life Science, Kyung Hee University, 1732, Deogyeong-daero, Giheung-gu, Yongin-si, Gyeonggi-do 17104, Republic of Korea.

出版信息

Photochem Photobiol Sci. 2018 Oct 10;17(10):1396-1408. doi: 10.1039/c8pp00174j.

DOI:10.1039/c8pp00174j
PMID:30225503
Abstract

Icariin (ICA) and icaritin (ICT) exhibit many pharmacological functions including anti-osteoporosis, anti-cardiovascular, and anti-cancer activities; however, there are few comprehensive studies that track the detailed effects on UVB-induced photoaging. The recovery effects of ICA and ICT were investigated in UVB-irradiated human keratinocytes (HaCaTs). The results indicated that ICT and ICA showed strong radical scavenging activity, and the reactive oxygen species (ROS) scavenging activity of ICT was superior. UVB-induced matrix metalloproteinase-1 (MMP-1) expression was blocked by ICA via the inhibition of mitogen-activated protein kinase/activator protein 1 (MAPK/AP-1), which directly reduced extracellular matrix (ECM) degradation. ICT activated nuclear factor erythroid 2 related factor 2 (Nrf2) to improve the anti-oxidative stress capacity and suppress nuclear factor-κB (NF-κB) activation, decreasing vascular endothelial growth factor (VEGF) protein, and inflammatory cytokines induced ECM degrading enzyme secretion. Moreover, ICT was more advantageous to improve transforming growth factor beta 1 (TGF-β1) and procollagen type I expression than ICA, promoting the synthesis of collagen. Therefore, ICA and ICT have potential to treat UVB-induced oxidative stress, inflammation and photoaging, and will be posited as a novel strategy to alleviate photodamage.

摘要

朝藿定(ICA)和朝藿定苷(ICT)具有多种药理作用,包括抗骨质疏松、抗心血管和抗癌作用;然而,很少有全面的研究跟踪其对 UVB 诱导的光老化的详细影响。本文研究了 ICA 和 ICT 对 UVB 照射的人角质形成细胞(HaCaTs)的恢复作用。结果表明,ICT 和 ICA 表现出很强的自由基清除活性,并且 ICT 的活性氧(ROS)清除活性更优。ICA 通过抑制丝裂原活化蛋白激酶/激活蛋白 1(MAPK/AP-1)阻断 UVB 诱导的基质金属蛋白酶-1(MMP-1)表达,直接减少细胞外基质(ECM)降解。ICT 通过激活核因子红细胞 2 相关因子 2(Nrf2)来提高抗氧化应激能力并抑制核因子-κB(NF-κB)的激活,减少血管内皮生长因子(VEGF)蛋白和炎症细胞因子诱导的 ECM 降解酶分泌。此外,ICT 比 ICA 更有利于提高转化生长因子 β1(TGF-β1)和 I 型前胶原的表达,促进胶原的合成。因此,ICA 和 ICT 具有治疗 UVB 诱导的氧化应激、炎症和光老化的潜力,并将被提出作为缓解光损伤的一种新策略。

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