| Specialized pro-resolving mediator 7S MaR1 inhibits IL-6 expression via modulating ROS/p38/ERK/NF-リB pathways in PM10-exposed keratinocytes |
Jinju Kim  1,# (Graduate student), Hyo-Min Park 1 (Graduate student), Chae-Min Lim 1 (Graduate student), Kyeong-Bae Jeon 1 (Graduate student), Seonhwa Kim 1 (Graduate student), Jin Lee1 (Graduate student), Jin-Tae Hong 2 (Professor), Deok-Kun Oh 1 (Professor), Young Yang 3 (Professor; Corresponding Author), Do-young Yoon 1,* (Professor; Corresponding Author) |
1Department of Bioscience and Biotechnology, Konkuk University, Seoul 05029, Korea,
2College of Pharmacy & Medical Research Center, Chungbuk National University, Cheongju 28160, Korea,
3Department of Biological Sciences, Sookmyung Women’s University, Seoul 04310, Korea |
|
Abstract
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-リB signaling pathways. These results demonstrate that PM10 induces inflammation by upregulating inflammatory cytokines, which can lead to skin diseases. In addition, 7S MaR1 can resolve inflammation caused by PM10-induced oxidative stress and inflammatory cytokines.
|
| Abstract, Accepted Manuscript [Submitted on August 4, 2024, Accepted on September 2, 2024] |
|