Restorative effects of camellia oil on the skin-barrier function in a model of DNCB-induced atopic dermatitis

This study aimed to evaluate the therapeutic efficacy of camellia oil on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD) in mice, as well as its effect on the expression of skin-barrier-related proteins. A mouse model of AD was created via topical application of DNCB; subsequently, t...

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Bibliographic Details
Main Authors: Shicheng Jiao, Lijun Deng, Mu Niu, Jie Yang
Format: Article
Language:English
Published: PAGEPress Publications 2025-01-01
Series:European Journal of Histochemistry
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Online Access:https://www.ejh.it/index.php/ejh/article/view/4147
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Summary:This study aimed to evaluate the therapeutic efficacy of camellia oil on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD) in mice, as well as its effect on the expression of skin-barrier-related proteins. A mouse model of AD was created via topical application of DNCB; subsequently, the animals were randomly divided into four groups: the blank control (Control), model (Model), moisturizing cream (Moisturizer), and camellia oil (Camellia) groups. The Camellia group received camellia oil, whereas the Moisturizer group was treated with moisturizing cream, as a positive control. Skin lesions, ear and back tissue morphology, and the serum levels of IgE, IL-4, and IFN-γ were analyzed. Compared with the Control group, AD mice exhibited erythema, papules, dryness, peeling, and significantly higher serum IgE and IL-4 levels. Compared with the Model group, treatment with camellia oil and moisturizing cream considerably reduced skin inflammation, ear thickness, and scratching frequency. A histopathological analysis revealed that camellia oil reduced inflammatory-cell infiltration and edema in the AD-affected skin. Furthermore, camellia oil upregulated filaggrin (FLG), thus aiding in skin-barrier repair. These findings suggest that camellia oil significantly improves AD symptoms, enhances FLG expression, and restores the damaged skin barrier in AD mouse models.
ISSN:1121-760X
2038-8306