Specialized pro-resolving mediator 7S MaR1 inhibits IL-6 expression via modulating ROS/p38/ERK/NF-B pathways in PM10-exposed keratinocytes
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초록
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 skindamages caused by PM. Here, we explored the protective effectof 7S MaR1, a specialized pro-resolving mediator derived fromdocosahexaenoic acid, on skin inflammation and the oxidativestress induced by PM with a diameter 10 m or less (PM10) inhuman keratinocyte HaCaT cells. Interestingly, PM10-inducedROS generation was modulated by 7S MaR1 via the recovery ofROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6expression via modulating the p38/ERK/NF-B signaling pathways. These results demonstrate that PM10 induces inflammatorycytokines, which can lead to skin diseases. In addition, 7S MaR1can resolve inflammation caused by PM10-induced oxidativestress and inflammatory cytokines.
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 skindamages caused by PM. Here, we explored the protective effectof 7S MaR1, a specialized pro-resolving mediator derived fromdocosahexaenoic acid, on skin inflammation and the oxidativestress induced by PM with a diameter 10 m or less (PM10) inhuman keratinocyte HaCaT cells. Interestingly, PM10-inducedROS generation was modulated by 7S MaR1 via the recovery ofROS scavenger genes. 7S MaR1 reduced PM10-induced IL-6expression via modulating the p38/ERK/NF-B signaling pathways. These results demonstrate that PM10 induces inflammatorycytokines, which can lead to skin diseases. In addition, 7S MaR1can resolve inflammation caused by PM10-induced oxidativestress and inflammatory cytokines.
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