Magnolol Reduces Atopic Dermatitis-like Symptoms in BALB/c Mice
In traditional Korean medicines, is commonly included for the remedy of atopic dermatitis, and magnolol is a major constituent of . Its pharmacological effects include anti-inflammatory, hepatoprotective, and antioxidant effects. Using BALB/c mice repeatedly exposed to 1-chloro-2,4-dinitrobenzene (D...
Saved in:
Published in | Life (Basel, Switzerland) Vol. 14; no. 3; p. 339 |
---|---|
Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Switzerland
MDPI AG
01.03.2024
MDPI |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | In traditional Korean medicines,
is commonly included for the remedy of atopic dermatitis, and magnolol is a major constituent of
. Its pharmacological effects include anti-inflammatory, hepatoprotective, and antioxidant effects. Using BALB/c mice repeatedly exposed to 1-chloro-2,4-dinitrobenzene (DNCB), magnolol was evaluated in atopic dermatitis-like lesions. Administration of magnolol (10 mg/kg, intraperitoneal injection) markedly relieved the skin lesion severity including cracking, edema, erythema, and excoriation, and significantly inhibited the increase in IgE levels in the peripheral blood. A DNCB-induced increase in mast cell accumulation in atopic dermatitis skin lesions was reversed by magnolol administration, as well as a rise in expression levels of pro-inflammatory Th2/Th17/Th1 cytokines' (IL-4, IL-13, IL-17A, IFN-γ, IL-12A, TARC, IL-8, and IL-6) mRNAs in the lymph nodes and skin (n = 5 per group). In lymph nodes, magnolol reversed DNCB's increase in CD4
RORγt
Th17 cell fraction and decrease in CD4
FoxP3
regulatory T cell fraction. The results also showed that magnolol suppressed T cell differentiation into Th17 and Th2 cells, but not Th1 cells. Magnolol suppresses atopic dermatitis-like responses in the lymph nodes and skin, suggesting that it may be feasible to use it as a treatment for atopic dermatitis through its suppression of Th2/Th17 differentiation. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2075-1729 2075-1729 |
DOI: | 10.3390/life14030339 |