Abstract

Dioscorea quinqueloba has been used for food substances, as well as in herbal medicines for allergic diseases such as asthma. This study aimed to investigate the anti-atopic dermatitis (AD) effects of the total extract of D. quinqueloba rhizomes and active fractionson murine oxazolone- and 2,4-dinitrochlorobenzene-induced models of AD. Specific AD symptoms, such as erythema, ear swelling, and epidermis thickening, were significantly reduced in the oxazolone-mediated AD BALB/c mice upon topical application of D. quinqueloba rhizomes 95% EtOH extract (DQ). DQEA (D. quinqueloba rhizomes EtOAc fraction) was beneficial for protecting the skin barrier against AD in DNCB-sensitized SKH-1 hairless mice. Decreased total serum IgE and IL-4 levels could be observed in atopic dorsal skin samples of the DQEA-treated group. On the basis of the phytochemical analysis, DQEA was found to contain dioscin and gracillin as its main compounds. Therapeutic applications with D. quinqueloba might be useful in the treatment of AD and related inflammatory skin diseases.

Highlights

  • Atopic dermatitis (AD) is a pruritic chronic inflammatory skin disease [1]

  • Mouse Ears erythema, and dryness were observed in the ears of oxazolone-challenged mice

  • Accordingwere to thesignificantly phenotypic observation, observed ear swelling and intensity by oxazolone reduced observation, ear swelling and erythematic intensity caused by oxazolone were significantly reduced when ears were exposed to 1% D. quinqueloba EtOH extract (DQ) for 21 days (Figure 1b)

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Summary

Introduction

Atopic dermatitis (AD) is a pruritic chronic inflammatory skin disease [1]. Atopic disease is triggered by a variety of allergic factors, including irritants, food, and stress factors [4]. Atopic dermatitis can be categorized into two types, including an extrinsic type (environmental or allergic AD) and an intrinsic type (genetic or non-allergic AD) [7]. Extrinsic AD is the classical type of AD, while the incidence of intrinsic AD is approximately 20% of patients [7,8]. Extrinsic or environmental triggers enhance IgE-mediated sensitization and allergic reaction, further contributing to severe forms of skin inflammation in AD [9]. Skin barrier damage contributes to the high serum IgE level, reduced

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