Abstract
Resveratrol-enriched rice (RR) was developed using genetic engineering to combine the properties of resveratrol and rice. To evaluate the effect of RR on pruritic skin inflammation in atopic dermatitis (AD)-like skin lesions, we used dinitrochlorobenzene (DNCB)-induced NC/Nga mice and an in vitro 3D skin model. Normal rice (NR), resveratrol, and RR were topically applied to mice dorsal skin, following which the dermatitis index and scratching frequency were calculated. Histological examination was performed by hematoxylin and eosin and immunohistochemistry staining of IL-31 level. The level of immunoglobulin E (IgE) and IL-31 in the serum was determined by enzyme-linked immunosorbent assay (ELISA). The cytotoxicity of RR and the expression levels of pro-inflammatory cytokines were also determined in cultured human keratinocytes and a 3D skin model. RR significantly reduced scratching frequency, decreased the dermatitis severity and trans-epidermal water loss (TEWL) and improved skin hydration in DNCB-induced NC/Nga mice. RR also significantly decreased serum IL-31 and IgE levels and suppressed the production of IL-6 in human keratinocytes and the 3D skin model. Our study indicates that the synergistic effect of rice and resveratrol manifested by the topical application of RR can serve as a potential alternative therapy for chronic skin inflammatory diseases such as AD.
Highlights
Atopic dermatitis (AD) is a chronic inflammatory skin disease that has been characterized by pruritic eczematous lesions and skin barrier dysfunction [1]
To assess the effect of Resveratrol-enriched rice (RR) against the development of AD-like skin lesions, NC/Nga mice were treated with Dexamethasone (Dex 0.1% (w/v)), normal rice extract (NR, 2.5% (w/v)), RR rice extract (RR, 2.5% (w/v)), and RSV (2.5% (w/v)) thrice weekly for five weeks after sensitization with 0.4% (w/v) DNCB (Figure 1A)
The Normal rice (NR), RR, and RSV treatments appeared capable of reducing AD severity, but RR treatment showed more recovery effect than NR treated group
Summary
Atopic dermatitis (AD) is a chronic inflammatory skin disease that has been characterized by pruritic eczematous lesions and skin barrier dysfunction [1]. AD affects up to 20% of children and 10% of adults in developed countries [2]. It develops from a complex interplay between genetic, environmental, and immunologic factors, which leads to multiple changes in the immune system [3]. The pathogenesis of AD is not yet fully understood, but the development of AD lesions is known to be associated with skin barrier dysfunction, cell-mediated immune response, and immunoglobulin E (IgE)-related hypersensitivity [4]. The imbalance in Th1/Th2-cytokines, observed in AD, promotes IgE-mediated hypersensitivity and itching. Repetitive itching and scratching are the major symptoms of AD; the itch-scratch cycle leads to loss of sleep and severely disturbs the quality of life of AD patients
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