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,Photochemical & Photobiological Sciences

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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
Photochemical & Photobiological Sciences ( IF 2.7 ) Pub Date : 2018-09-10 00:00:00 , DOI: 10.1039/c8pp00174j
Eunson Hwang _{1,

2,

3,

4} , Pei Lin _{1,

2,

3,

4} , Hien T. T. Ngo _{1,

2,

3,

4} , Wei Gao _{1,

2,

3,

4} , Yu-Shuai Wang _{1,

2,

3,

4} , Hong-Shan Yu _{5,

6,

7,

8} , Tae-Hoo Yi _{1,

2,

3,

4}

Affiliation

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.

中文翻译：

伊卡瑞汀和伊卡瑞汀通过刺激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照射的人角质形成细胞的比较研究

伊卡瑞汀（ICA）和伊卡瑞汀（ICT）具有许多药理功能，包括抗骨质疏松症，抗心血管和抗癌活性。然而，很少有综合研究追踪对UVB诱导的光老化的详细影响。研究了ICA和ICT在UVB辐射的人角质形成细胞（HaCaTs）中的恢复作用。结果表明，ICT和ICA显示出较强的自由基清除活性，而ICT的活性氧（ROS）清除活性更高。UVB诱导的基质金属蛋白酶-1（MMP-1）表达被ICA通过阻断抑制有丝分裂原激活的蛋白激酶/激活蛋白1（MAPK / AP-1），可直接减少细胞外基质（ECM）的降解。ICT激活核因子红系2相关因子2（Nrf2）以提高抗氧化应激能力并抑制核因子-κB（NF-κB）激活，降低血管内皮生长因子（VEGF）蛋白，以及炎性细胞因子诱导的ECM降解酶分泌。此外，与ICA相比，ICT更有利于改善转化生长因子β1（TGF-β1）和I型胶原蛋白的表达，从而促进胶原蛋白的合成。因此，ICA和ICT在治疗UVB引起的氧化应激，炎症和光老化方面具有潜力，将被认为是减轻光损伤的新策略。

更新日期：2018-09-10

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