Shirato Ken, Koda Tomoko, Takanari Jun, Sakurai Takuya, Ogasawara Junetsu, Imaizumi Kazuhiko, Ohno Hideki, Kizaki Takako
Department of Molecular Predictive Medicine and Sport Science, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo 181-8611, Japan.
Faculty of Nursing, Tokyo Healthcare University, 2-5-1 Higashigaoka, Meguro, Tokyo 152-8558, Japan.
Evid Based Complement Alternat Med. 2018 Jun 3;2018:5072986. doi: 10.1155/2018/5072986. eCollection 2018.
Ultraviolet (UV) irradiation induces proinflammatory responses in skin cells, including dermal fibroblasts, accelerating premature skin aging (photoaging). ETAS 50, a standardized extract from the stem, is a novel and unique functional food that suppresses proinflammatory responses of hydrogen peroxide-stimulated skin fibroblasts and interleukin- (IL-) 1-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-B (IB) protein and increased levels of nuclear p65 protein. The nuclear factor-B nuclear translocation inhibitor JSH-23 abolished UV-B irradiation-induced IL-1 mRNA expression, indicating that p65 regulates transcriptional induction. ETAS 50 also markedly suppressed UV-B irradiation-induced increases in IL-1 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- protein levels in the nucleus without recovering cytosolic IB 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.
紫外线（UV）照射可诱导皮肤细胞（包括真皮成纤维细胞）产生促炎反应，加速皮肤过早衰老（光老化）。ETAS 50是一种从茎中提取的标准化提取物，是一种新型且独特的功能性食品，可抑制过氧化氢刺激的皮肤成纤维细胞和白细胞介素-（IL-）1刺激的肝细胞的促炎反应。为了阐明其抗光老化潜力，我们研究了UV-B照射后ETAS 50处理是否能减弱正常人皮肤成纤维细胞（NHDFs）的促炎反应。UV-B照射的NHDFs显示细胞质中核因子-κB（NF-κB）抑制蛋白IκB的水平降低，而细胞核中p65蛋白的水平升高。核因子-κB核转位抑制剂JSH-23消除了UV-B照射诱导的IL-1 mRNA表达，表明p65调节转录诱导。ETAS 50也显著抑制了UV-B照射诱导的IL-1 mRNA水平的升高。免疫荧光分析显示，UV-B照射后ETAS 50使p65保留在细胞质中。蛋白质印迹法也表明ETAS 50抑制了UV-B照射诱导的细胞核中p65蛋白的增加。此外，ETAS 50明显抑制了UV-B照射诱导的细胞核中输入蛋白-α水平的分布，而未恢复细胞质中IκB蛋白的水平。这些结果表明，ETAS 50通过抑制p65的核输入机制对UV-B照射的NHDFs发挥抗炎作用。因此，ETAS 50可能通过抑制紫外线照射诱导的真皮成纤维细胞促炎反应来预防光老化。
