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 Eun; Budluang, Phatcharaporn; Park, Jumin; Lee, Kon Ho; Pakdeepromma, Sirichatnach; Kaewpiboon, Chutima; Kang, Ho Young; Hwang, Dae Youn; Chung, 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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