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

Küçük Resim Yok

Tarih

2020

Dergi Başlığı

Dergi ISSN

Cilt Başlığı

Yayıncı

Mary Ann Liebert, Inc

Erişim Hakkı

info:eu-repo/semantics/openAccess

Özet

Background: 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.

Açıklama

Anahtar Kelimeler

Atopic Dermatitis, Inflammation, Quercetin, Keratinocyte, Wound Healing, Thymic Stromal Lymphopoietin, Stem-Cell Survival, Epithelial-Cells, Tnf-Alpha, In-Vitro, Skin, Migration, Expression, Cytokines, Activation

Kaynak

Pediatric Allergy Immunology And Pulmonology

WoS Q Değeri

Q4

Scopus Q Değeri

Q3

Cilt

33

Sayı

2

Künye