Quercetin Improves Inflammation, Oxidative Stress, and Impaired Wound Healing in Atopic Dermatitis Model of Human Keratinocytes

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dc.authoridBeken, Burcin/0000-0001-7677-7690
dc.authoridSERTTAS, RIZA/0000-0002-7493-0388
dc.authorwosidYazicioglu, Mehtap/AAB-9587-2022
dc.authorwosidBeken, Burcin/GPK-8389-2022
dc.authorwosidSERTTAS, RIZA/AAG-7463-2020
dc.contributor.authorBeken, Burcin
dc.contributor.authorSerttas, Riza
dc.contributor.authorYazicioglu, Mehtap
dc.contributor.authorTurkekul, Kader
dc.contributor.authorErdogan, Suat
dc.date.accessioned2024-06-12T10:52:47Z
dc.date.available2024-06-12T10:52:47Z
dc.date.issued2020
dc.departmentTrakya Üniversitesien_US
dc.description.abstractBackground: 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.en_US
dc.description.sponsorshipTrakya University Scientific Research Projects Unit (TUBAP) [2019-89]en_US
dc.description.sponsorshipThis study was funded by Trakya University Scientific Research Projects Unit (TUBAP) (Project number: 2019-89).en_US
dc.identifier.doi10.1089/ped.2019.1137
dc.identifier.endpage79en_US
dc.identifier.issn2151-321X
dc.identifier.issn2151-3228
dc.identifier.issue2en_US
dc.identifier.pmid34678092en_US
dc.identifier.scopus2-s2.0-85086932354en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage69en_US
dc.identifier.urihttps://doi.org/10.1089/ped.2019.1137
dc.identifier.urihttps://hdl.handle.net/20.500.14551/18837
dc.identifier.volume33en_US
dc.identifier.wosWOS:000536290200001en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherMary Ann Liebert, Incen_US
dc.relation.ispartofPediatric Allergy Immunology And Pulmonologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAtopic Dermatitisen_US
dc.subjectInflammationen_US
dc.subjectQuercetinen_US
dc.subjectKeratinocyteen_US
dc.subjectWound Healingen_US
dc.subjectThymic Stromal Lymphopoietinen_US
dc.subjectStem-Cell Survivalen_US
dc.subjectEpithelial-Cellsen_US
dc.subjectTnf-Alphaen_US
dc.subjectIn-Vitroen_US
dc.subjectSkinen_US
dc.subjectMigrationen_US
dc.subjectExpressionen_US
dc.subjectCytokinesen_US
dc.subjectActivationen_US
dc.titleQuercetin Improves Inflammation, Oxidative Stress, and Impaired Wound Healing in Atopic Dermatitis Model of Human Keratinocytesen_US
dc.typeArticleen_US

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