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Cited 2 time in webofscience Cited 3 time in scopus
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N-benzyl-N-methyldecan-1-amine, derived from garlic, and its derivative alleviate 2,4-dinitrochlorobenzene-induced atopic dermatitis-like skin lesions in miceopen access

Authors
Kim, Ji EunBudluang, PhatcharapornPark, JuminLee, Kon HoPakdeepromma, SirichatnachKaewpiboon, ChutimaKang, Ho YoungHwang, Dae YounChung, Young-Hwa
Issue Date
Mar-2024
Publisher
Nature Research
Keywords
2,4-Dinitrochlorobenzene; Atopic dermatitis; IgE titer; Inflammation; Mast cells; N-benzyl-N-methyldecan-1-amine
Citation
Scientific Reports, v.14, no.1
Indexed
SCIE
SCOPUS
Journal Title
Scientific Reports
Volume
14
Number
1
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/70102
DOI
10.1038/s41598-024-56496-2
ISSN
2045-2322
Abstract
Given the intricate etiology and pathogenesis of atopic dermatitis (AD), the complete cure of AD remains challenging. This study aimed to investigate if topically applying N-benzyl-N-methyldecan-1-amine (BMDA), derived from garlic, and its derivative [decyl-(4-methoxy-benzyl)-methyl-1-amine] (DMMA) could effectively alleviate AD-like skin lesions in 2,4-dinitrochlorobenzene (DNCB)-treated mice. Administering these compounds to the irritated skin of DNCB-treated mice significantly reduced swelling, rash, and excoriation severity, alongside a corresponding decrease in inflamed epidermis and dermis. Moreover, they inhibited spleen and lymph node enlargement and showed fewer infiltrated mast cells in the epidermis and dermis through toluidine-blue staining. Additionally, they led to a lower IgE titer in mouse sera as determined by ELISA, compared to vehicle treatment. Analyzing skin tissue from the mice revealed decreased transcript levels of inflammatory cytokines (TNF-α, IL-1β, and IL-6), IL-4, iNOS, and COX-2, compared to control mice. Simultaneously, the compounds impeded the activation of inflammation-related signaling molecules such as JNK, p38 MAPK, and NF-κB in the mouse skin. In summary, these findings suggest that BMDA and DMMA hold the potential to be developed as a novel treatment for healing inflammatory AD. © The Author(s) 2024.
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