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Membrane-free stem cell components ameliorate atopic dermatitis in 2,4-dinitrochlorobenzene-induced NC/Nga miceopen access

Authors
Stalin, NattanLee, DongyupSharma, AmiteshDevi, ShivaniChoi, JiwonHwang, YunbhinKim, Young SilPark, Tae-Sik
Issue Date
Oct-2023
Publisher
WOLTERS KLUWER MEDKNOW PUBLICATIONS
Keywords
Atopic dermatitis; cytokine; inflammation; skin barrier; skin; stem cell
Citation
DERMATOLOGICA SINICA, v.41, no.4, pp 238 - 250
Pages
13
Journal Title
DERMATOLOGICA SINICA
Volume
41
Number
4
Start Page
238
End Page
250
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/90353
DOI
10.4103/ds.DS-D-23-00070
ISSN
1027-8117
2223-330X
Abstract
Background: Atopic dermatitis (AD) is a prevalent inflammatory skin disorder characterized by skin barrier dysfunction, thymic stromal lymphopoietin (TSLP) production and an imbalance in the Th1/Th2 immune response. While numerous studies have examined the therapeutic potential of adipose-derived stem cells (ADSC) in repairing and regenerating damaged skin tissues caused by AD, the effects of membrane-free stem cell components derived from ADSC extract (ADSCE) on AD have not been investigated. Objectives: The objective of this study was to investigate the alleviating effects of ADSCE on AD in mice and validate the therapeutic application of ADSCE on AD. Methods: An AD-like lesion was induced by the administration of 2,4-dinitrochlorobenzene (DNCB) on the dorsal skin of NC/Nga mice. Then, ADSCE was administered subcutaneously for 3 weeks. Dermatitis score, epidermal thickness, transepidermal water loss (TEWL), and serum levels of immunoglobulin E (IgE) were measured. Expression of the skin barrier proteins and inflammatory cytokines were measured by western blotting and quantitative real-time polymerase chain reaction. Results: The administration of ADSCE demonstrated a significant amelioration in several skin diseases, as indicated by improvements in dermatitis score, epidermal thickness, TEWL, and total blood levels of IgE. ADSCE treatment led to an upregulation in the expression of various skin barrier proteins, including involucrin, loricrin, occludin, and zonula occludens-1. In addition, ADSCE inhibited the infiltration of mast cells and the expression of TSLP. Expression of inflammatory cytokines, including tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-4, and inducible nitric oxide synthase, was also lowered by ADSCE. Conclusions: The use of ADSCE resulted in enhanced skin features and exerted anti-inflammatory properties on AD-like lesions in mice.
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