Abstract

Atopic dermatitis is an inflammatory and chronically relapsing skin disorder that commonly occurs in children; the number of atopic dermatitis patients is increasing. The cause and mechanism of atopic dermatitis have not been defined clearly, although many studies are ongoing. Epidemiological studies suggest that soybean and its isoflavones have immunoregulatory activities. Here, we report that 7,3′,4′-trihydroxyisoflavone (7,3′,4′-THIF), a major metabolite of daidzin, effectively inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 production in RAW 264.7 cells, and also reduced β-hexosaminidase secretion in RBL-2H3 cells. Moreover, 7,3′,4′-THIF significantly reduced scratching time, transepidermal water loss, and mast cell infiltration. It also decreased protease-activated receptor (PAR)-2 and IL-4 expression and increased filaggrin expression in skin lesions of NC/Nga mice. These results suggest that 7,3′,4′-THIF improves Dermatophagoides farina body extract-induced atopic dermatitis in NC/Nga mice.

Highlights

  • Atopic dermatitis (AD) is a chronically relapsing skin disorder that presents with severe itching and inflammation [1,2,3]

  • Anti-mouse antibodies against filaggrin and protease-activated receptor (PAR)-2 for immunohistochemistry were purchased from Santa Cruz Biotechnology, Inc. (Dallas, Texas, USA); an antibody against IL-4 was purchased from ProSpec (EB, NJ, USA)

  • The results suggest that consuming soy products abundant in isoflavones significantly reduced symptoms of allergic rhinitis [23]. 7,3󸀠,4󸀠-THIF is a major metabolite of daidzein that is produced by hydroxylation of its 3󸀠 carbon

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Summary

Introduction

Atopic dermatitis (AD) is a chronically relapsing skin disorder that presents with severe itching and inflammation [1,2,3]. It commonly occurs in children and infants, and its incidence is increasing globally [3, 4]. Levels of various inflammatory mediators, including tumor necrosis factor (TNF)-α, nitric oxide (NO), and IL6, are high in the skin of patients with AD [5]. When allergens invade an AD skin lesion, invading allergen binds to specific IgE on the surface of mast cells or basophils and activates them to secrete substances such as histamine that are associated with allergic reactions [6]. Β-hexosaminidase is secreted from mast cells together with histamine and can be a marker of mast cell activation [7]

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