Abstract
To investigate the potential effects of acorn shells on atopic dermatitis (AD), we utilized oxazolone (OX)- or 2,4-dinitrochlorobenzene (DNCB)-induced AD-like lesion mouse models. Our research demonstrates that Acorn shell extract (ASE) improved the progression of AD-like lesions, including swelling, which were induced by oxazolone on Balb/c mouse ears. Additionally, ASE significantly decreased the ear thickness (OX: 0.42 ± 0.01 mm, OX-ASE: 0.32 ± 0.02 mm) and epidermal thickness (OX: 75.3 ± 32.6 µm, OX-ASE: 46.1 ± 13.4 µm). The continuous DNCB-induced AD mouse model in SKH-1 hairless mice demonstrated that ASE improved AD-like symptoms, including the recovery of skin barrier dysfunction, Immunoglobulin E hyperproduction (DNCB: 340.1 ± 66.8 ng/mL, DNCB-ASE: 234.8 ± 32.9 ng/mL) and an increase in epidermal thickness (DNCB: 96.4 ± 21.9 µm, DNCB-ASE: 52.4 ± 16.3 µm). In addition, we found that ASE suppressed the levels of AD-involved cytokines, such as Tumor Necrosis Factor α, IL-1β, IL-25 and IL-33 in both animal models. Furthermore, gallic acid and ellagic acid isolated from ASE suppressed β-hexosaminidase release and IL-4 expression in RBL-2H3 cells. The acorn shell and its active phytochemicals have potential as a new remedy for the improvement of atopic dermatitis and other inflammatory diseases.
Highlights
Atopic dermatitis (AD) is a chronic inflammatory skin disease with symptoms including lesions from severe pruritus, epidermal hyperplasia, edema, erythema and erythematous plaque [1,2].The cause of atopic dermatitis (AD) has not yet been identified, but genetic factors, immune function imbalance and environmental factors are known to be involved [3,4]
Interleukin 4 (IL-4) is known to play an important role for IgE hyperproduction which occurs at the onset of atopic dermatitis [33,34]
We proved the improved effects of Acorn shell extract (ASE) on atopic dermatitis (AD) by oxazolone (OX)- or 2,4-dinitrochlorobenzene (DNCB)-induced AD-like lesion mouse models
Summary
Atopic dermatitis (AD) is a chronic inflammatory skin disease with symptoms including lesions from severe pruritus, epidermal hyperplasia, edema, erythema and erythematous plaque [1,2]. The cause of AD has not yet been identified, but genetic factors, immune function imbalance and environmental factors are known to be involved [3,4]. Activation of T lymphocytes, abnormalities in the cytokine system, decreases in cell mediated immunity and increases in IgE, have been reported to play an important role in the pathology of AD [5]. Atopic skin inflammation is regulated by diverse inflammatory cytokines. The cytokines Interleukin 4 (IL-4), IL-5 and IL-13 are hyperproduced in AD patients compared with healthy patients, and IL-4 and Interferon-γ are clearly increased in acute AD [6,7]
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