Anti-Inflammatory Effect of ETAS®50 by Inhibiting Nuclear Factor-κB p65 Nuclear Import in Ultraviolet-B-Irradiated Normal Human Dermal Fibroblasts.
Anti-Inflammatory Effect of ETAS®50 by Inhibiting Nuclear Factor-κB p65 Nuclear Import in Ultraviolet-B-Irradiated Normal Human Dermal Fibroblasts.
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DOI：
10.1155/2018/5072986
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Kizaki T
中科院分区：
文献类型：
--
作者：
Shirato K;Koda T;Takanari J;Sakurai T;Ogasawara J;Imaizumi K;Ohno H;Kizaki T
紫外线(UV)照射会在皮肤细胞中诱导促炎反应，包括真皮成纤维细胞，从而加速皮肤过早老化(光老化)。ETAS 50是一种从芦笋茎中提取的标准化提取物，是一种新颖而独特的功能食品，可抑制过氧化氢刺激的皮肤成纤维细胞和白细胞介素1β刺激的肝细胞的促炎反应。为了阐明其抗光老化的能力，我们检测了UV-B照射后ETAS 50处理是否减轻了正常人真皮成纤维细胞(NHDF)的促炎反应。UV-B辐射的NHDF细胞胞质核因子抑制物-κBα(IκBα)蛋白水平降低，核p65蛋白水平升高。核因子-κB核转位抑制剂JSH-23可阻断UV-B辐射诱导的IL-1β的表达，表明p65调控转录诱导。ETAS50还能显著抑制UV-B辐射诱导的IL-1β表达水平的升高。免疫荧光分析表明，经UV-B照射后，ETAS-50在胞浆中保留了p65。Western blotting还显示，ETAS 50抑制了UV-B辐射诱导的核p65蛋白表达的增加。此外，ETAS50明显抑制UV-B辐射诱导的Importin-α蛋白在细胞核内的分布，但不能恢复胞浆I-κBα蛋白水平。这些结果提示，ETAS50对UV-B辐射的NHDF具有抗炎作用，其机制可能是通过抑制p65的核输入机制实现的。因此，ETAS 50可能通过抑制紫外线辐射诱导的真皮成纤维细胞的促炎反应来预防光老化。
Ultraviolet (UV) irradiation induces proinflammatory responses in skin cells, including dermal fibroblasts, accelerating premature skin aging (photoaging). ETAS 50, a standardized extract from the Asparagus officinalis stem, is a novel and unique functional food that suppresses proinflammatory responses of hydrogen peroxide-stimulated skin fibroblasts and interleukin- (IL-) 1β-stimulated hepatocytes. To elucidate its antiphotoaging potencies, we examined whether ETAS 50 treatment after UV-B irradiation attenuates proinflammatory responses of normal human dermal fibroblasts (NHDFs). UV-B-irradiated NHDFs showed reduced levels of the cytosolic inhibitor of nuclear factor-κB α (IκBα) protein and increased levels of nuclear p65 protein. The nuclear factor-κB nuclear translocation inhibitor JSH-23 abolished UV-B irradiation-induced IL-1β mRNA expression, indicating that p65 regulates transcriptional induction. ETAS 50 also markedly suppressed UV-B irradiation-induced increases in IL-1β mRNA levels. Immunofluorescence analysis revealed that ETAS 50 retained p65 in the cytosol after UV-B irradiation. Western blotting also showed that ETAS 50 suppressed the UV-B irradiation-induced increases in nuclear p65 protein. Moreover, ETAS 50 clearly suppressed UV-B irradiation-induced distribution of importin-α protein levels in the nucleus without recovering cytosolic IκBα protein levels. These results suggest that ETAS 50 exerts anti-inflammatory effects on UV-B-irradiated NHDFs by suppressing the nuclear import machinery of p65. Therefore, ETAS 50 may prevent photoaging by suppressing UV irradiation-induced proinflammatory responses of dermal fibroblasts.
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影响因子：
4.8
作者：
Fagerlund, Riku;Melen, Krister;Julkunen, Ilkka
通讯作者：
Julkunen, Ilkka
影响因子：
3.6
作者：
Ahn, Byul-Nim;Kim, Jung-Ae;Kim, Se-Kwon
通讯作者：
Kim, Se-Kwon
DOI：
10.1042/bj20141186
发表时间：
2015-02-15
期刊：
The Biochemical journal
影响因子：
--
作者：
Pumroy RA;Cingolani G
通讯作者：
Cingolani G
影响因子：
1.8
作者：
Koda, Tomoko;Takanari, Jun;Imai, Hideki
通讯作者：
Imai, Hideki
DOI：
10.1038/jidsymp.2009.11
发表时间：
2009-08-01
影响因子：
--
作者：
Imokawa, Genji
通讯作者：
Imokawa, Genji