Kim Jinju, Park Hyo-Min, Lim Chae-Min, Jeon Kyeong-Bae, Kim Seonhwa, Lee Jin, Lee Jin, Hong Jin-Tae, Oh Deok-Kun, Yang Young, Yoon Do-Young
Department of Bioscience and Biotechnology, Konkuk University, Seoul 05029, Korea.
College of Pharmacy & Medical Research Center, Chungbuk National University, Cheongju 28160, Korea.
BMB Rep. 2024 Nov;57(11):490-496. doi: 10.5483/BMBRep.2024-0124.
Keratinocytes are susceptible to airborne particulate matter (PM) exposure, resulting in human skin barrier dysfunction. Therefore, it is important to find useful reagents to resolve skin damages caused by PM. Here, we explored the protective effect of 7S MaR1, a specialized pro-resolving mediator derived from docosahexaenoic acid, on skin inflammation and the oxidative stress induced by PM with a diameter 10 μm or less (PM10) in human keratinocyte HaCaT cells. Interestingly, PM10-induced ROS generation was modulated by 7S MaR1 via the recovery of ROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6 expression via modulating the p38/ERK/NF-κB signaling pathways. These results demonstrate that PM induces inflammatory cytokines, which can lead to skin diseases. In addition, 7S MaR1 can resolve inflammation caused by PM-induced oxidative stress and inflammatory cytokines. [BMB Reports 2024; 57(11): 490-496].
角质形成细胞易受空气中颗粒物(PM)暴露的影响,从而导致人体皮肤屏障功能障碍。因此,寻找有效的试剂来解决由PM引起的皮肤损伤非常重要。在此,我们探讨了7S MaR1(一种源自二十二碳六烯酸的特殊促消退介质)对人角质形成细胞HaCaT中由直径10μm或更小的PM(PM10)诱导的皮肤炎症和氧化应激的保护作用。有趣的是,7S MaR1通过恢复ROS清除基因来调节PM10诱导的ROS生成。7S MaR1通过调节p38/ERK/NF-κB信号通路降低PM10诱导的IL-6表达。这些结果表明,PM会诱导炎性细胞因子,进而导致皮肤疾病。此外,7S MaR1可以解决由PM诱导的氧化应激和炎性细胞因子引起的炎症。[《BMB报告》2024年;57(11): 490 - 496]