Beken, BurcinSerttas, RizaYazicioglu, MehtapTurkekul, KaderErdogan, Suat2024-06-122024-06-1220202151-321X2151-3228https://doi.org/10.1089/ped.2019.1137https://hdl.handle.net/20.500.14551/18837Background: Atopic dermatitis (AD) is a common inflammatory skin disease with complex pathogenesis. Natural flavonoids exhibit strong anti-inflammatory and antioxidant properties in many human diseases. In this study, the potential bioactive effect of quercetin, a polyphenolic plant-derived flavonoid, on the AD model of human keratinocytes was evaluated. Methods: Immortalized human HaCaT keratinocytes were treated with interleukin (IL) -4, -13, and tumor necrosis factor-alpha to mimic AD features in vitro. Then effects of quercetin on inflammation, oxidative stress, and wound healing were assessed. Results: Pretreatment of the cells with 1.5 mu M of quercetin significantly reduced the expression of AD-induced IL-1 beta, IL-6, IL-8, and thymic stromal lymphopoietin, while it strongly enhanced the expression of superoxide dismutase-1 (SOD1), SOD2, catalase, glutathione peroxidase, and IL-10. Quercetin promoted wound healing by inducing epithelial-mesenchymal transition, which was supported by the upregulation of Twist and Snail mRNA expression. Unexpectedly, quercetin pretreatment of AD-induced cells upregulated the mRNA expression of occludin and E-cadherin, while downregulating matrix metalloproteinase 1 (MMP1), MMP2, and MMP9 expression. The pretreatment inhibited AD-induced phosphorylation of extracellular signal-regulated kinase 1/2/mitogen-activated protein kinase (ERK1/2 MAPK) and the expression of nuclear factor-kappa B (NF-kappa B), but it did not alter signal transducer and activator of transcription 6 (STAT6) phosphorylation. Conclusion: Quercetin may serve as a potential bioactive substance for atopic dermatitis-related symptoms through anti-inflammatory and antioxidant activities along with its acceleration of wound healing via ERK1/2 MAPK and NF-kappa B pathways.en10.1089/ped.2019.1137info:eu-repo/semantics/openAccessAtopic DermatitisInflammationQuercetinKeratinocyteWound HealingThymic Stromal LymphopoietinStem-Cell SurvivalEpithelial-CellsTnf-AlphaIn-VitroSkinMigrationExpressionCytokinesActivationQuercetin Improves Inflammation, Oxidative Stress, and Impaired Wound Healing in Atopic Dermatitis Model of Human KeratinocytesArticle3326979Q4WOS:0005362902000012-s2.0-8508693235434678092Q3