Effects of Angelica gigas Nakai as an Anti-Inflammatory Agent in In Vitro and In Vivo Atopic Dermatitis Models.

Seon Ok,Tae-Sung Jung,Ji-wook Jung,Sa-Rang Oh,Deok-Seon Ryu,Sang-Ok Jeon

doi:10.1155/2018/2450712

Abstract

We investigated the cellular and molecular mechanisms mediating the effects of Angelica gigas Nakai extract (AGNE) through the mitogen-activated protein kinases (MAPKs)/NF-κB pathway using in vitro and in vivo atopic dermatitis (AD) models. We examined the effects of AGNE on the expression of proinflammatory cytokines and chemokines in human mast cell line-1 (HMC-1) cells. Compound 48/80-induced pruritus and 2,4-dinitrochlorobenzene- (DNCB-) induced AD-like skin lesion mouse models were also used to investigate the antiallergic effects of AGNE. AGNE reduced histamine secretion, production of proinflammatory cytokines including interleukin- (IL-) 1β, IL-4, IL-6, IL-8, and IL-10, and expression of cyclooxygenase- (COX-) 2 in HMC-1 cells. Scratching behavior and DNCB-induced AD-like skin lesions were also attenuated by AGNE administration through the reduction of serum IgE, histamine, tumor necrosis factor-α (TNF-α), IL-6 levels, and COX-2 expression in skin tissue from mouse models. Furthermore, these inhibitory effects were mediated by the blockade of the MAPKs and NF-κB pathway. The findings of this study proved that AGNE improves the scratching behavior and atopy symptoms and reduces the activity of various atopy-related mediators in HMC-1 cells and mice model. These results suggest the AGNE has a therapeutic potential in anti-AD.

Highlights

Atopic dermatitis (AD) is a chronic inflammatory dermatitis disease characterized by severe itching, eczematous skin eruption, asteatosis, and red, swollen, and cracked skin [1]
We investigated the effect of increasing concentrations of Angelica gigas Nakai extract (AGNE) on histamine release from PMACI-induced HMC-1 cells
Histamine release was enhanced in PMACI-stimulated cells compared to that of the control cells, but AGNE-treated cells showed a higher decrease in histamine release than PMACI-induced human mast cell line-1 (HMC1) cells did

Summary

Introduction

Atopic dermatitis (AD) is a chronic inflammatory dermatitis disease characterized by severe itching, eczematous skin eruption, asteatosis, and red, swollen, and cracked skin [1]. The general pathogenesis of AD has not been unknown, but AD-related symptoms including repeated worsening or recurrence are primarily assumed to be caused by two reasons. An association between AD and IgE has been proven by the evidence that serum IgE increases in proportion to the symptoms of eczema, asthma, and allergic rhinitis. Serum IgE level has been shown to increase in basophils after exposure to antigens and the existence of an IgE receptor has been demonstrated in mast cell and basophils. This phenomenon is referred to as the “IgE-mediated sensitization.”. Th1 cells primarily produce interferon- (INF-) γ and tumor necrosis factor-α (TNF-α), which are required for cell-mediated inflammatory reactions while Th2 cells secrete IL-4, IL-5, IL-10, and IL-13, which mediate B cell activation

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