Dieckol Inhibits the Effects of Particulate Matter 10 on Sebocytes, Outer Root Sheath Cells, and Cutibacterium Acnes−Pretreated Mice
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Background: Particulate matter (PM) is an air pollutant that can impair the human skin. Antioxidants have been tested to improve PM-induced skin inflammation. Objective: In this study, we investigated the effects of dieckol on PM-induced inflammation on cultured human sebocytes, outer root sheath (ORS) cells, and mice pretreated with Cuti- bacterium acnes Methods: We cultured and treated the sebocytes and ORS cells with 5 μM of dieckol and 100 μg/ml of PM10 for 24 h. The −pretreated mice received 5 μM of dieckol and 100 μg/ml of PM10. We measured cell viability using MTT assay. Real-time PCR and mea- surement of reactive oxygen species (ROS) and sebum production analyzed the effects. Results: Dieckol inhibited the upregulation of the gene expression of the inflammatory cytokines, matrix metalloproteinase (MMP), aryl hydrocarbon receptor, and nuclear fac- tor kappa-light-chain-enhancer of activated B cells by PM10 in the cultured sebocytes and ORS cells and inhibited an increase in ROS production by PM10 in the cultured sebocytes. In addition, dieckol decreased the inflammatory cytokines, MMP, and sebum production in −pretreated mice. Conclusion: Dieckol effectively reduced the expression of inflammatory biomarkers and the production of sebum in cultured sebocytes, ORS cells, and C. acne−pretreated mice.
Abstract
Background: Particulate matter (PM) is an air pollutant that can impair the human skin. Antioxidants have been tested to improve PM-induced skin inflammation. Objective: In this study, we investigated the effects of dieckol on PM-induced inflammation on cultured human sebocytes, outer root sheath (ORS) cells, and mice pretreated with Cuti- bacterium acnes Methods: We cultured and treated the sebocytes and ORS cells with 5 μM of dieckol and 100 μg/ml of PM10 for 24 h. The −pretreated mice received 5 μM of dieckol and 100 μg/ml of PM10. We measured cell viability using MTT assay. Real-time PCR and mea- surement of reactive oxygen species (ROS) and sebum production analyzed the effects. Results: Dieckol inhibited the upregulation of the gene expression of the inflammatory cytokines, matrix metalloproteinase (MMP), aryl hydrocarbon receptor, and nuclear fac- tor kappa-light-chain-enhancer of activated B cells by PM10 in the cultured sebocytes and ORS cells and inhibited an increase in ROS production by PM10 in the cultured sebocytes. In addition, dieckol decreased the inflammatory cytokines, MMP, and sebum production in −pretreated mice. Conclusion: Dieckol effectively reduced the expression of inflammatory biomarkers and the production of sebum in cultured sebocytes, ORS cells, and C. acne−pretreated mice.
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