Abstract

Rhus verniciflua Stokes (RV) has traditionally been used as a food supplement and a traditional herbal medicine for centuries in Korea. Recent studies suggest that RV has potent antioxidative, antitumor, and anti-inflammatory properties. In this study, the anti-inflammatory effects of RV from mice sensitized with 2,4-dinitrofluorobenzene (DNFB) and activated macrophages were investigated. The results showed that RV reduced ear swelling and hyperplasia of ear tissue as well as an increase in vascular permeability, which are characteristics of allergic contact dermatitis (ACD) with evident histomorphological changes in epidermis and dermis. Decreased numbers of infiltrated mast cells were seen in RV extract treated group, using toluidine blue staining. RV extract significantly regulates the expression of inducible nitric oxide synthase (iNOS) at the translational level in activated macrophages. Furthermore, RV extract and its active compound, fisetin, attenuated the level of tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) mRNA in LPS-stimulated macrophages. Anti-ACD effect of RV extract may be due to the suppression of iNOS and proinflammatory cytokines which might be mediated via the NFκB signaling pathways. Collectively, RV extract has potential for alleviating ACD-like symptoms induced by DNFB in the mouse.

Highlights

  • Allergic contact dermatitis (ACD) is a highly prevalent skin inflammatory disease and is characterized by allergic signs and symptoms of the skin, such as redness, edema, warmth, and pruritus, accompanied with scaling and dryness [1]

  • Effect of Rhus verniciflua Stokes (RV) Extract on the Vascular Permeability and Ear Swelling in DNFB-Induced Allergic Contact Dermatitis (ACD) Mice

  • In order to explore a therapeutic role of RV extract in skin inflammatory diseases in vivo, we employed a mouse model of allergic contact dermatitis

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Summary

Introduction

Allergic contact dermatitis (ACD) is a highly prevalent skin inflammatory disease and is characterized by allergic signs and symptoms of the skin, such as redness, edema, warmth, and pruritus, accompanied with scaling and dryness [1]. The challenge phase of CD occurs when sensitized individual is exposed to the same hapten, which recruits effector T cells and triggers the inflammatory process [2]. Study of the pathophysiology of ACD is derived mainly from animal models in which the skin inflammation is caused by repeated topical application to the haptens. Among these haptens, 2,4-dinitrofluorobenzene (DNFB) is known to mediate allergic contact dermatitis by CD8+ cytotoxic T cells and mast cells and is used to produce skin contact hypersensitivity in mice models [3]. Numerous lines of evidence describe that activated macrophages play a crucial role in inflammatory process through producing proinflammatory cytokines and mediators

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