Anti‑inflammatory effect of Amomum xanthioides in a mouse atopic dermatitis model

Choi,Young‑Ae; Choi,Jin  Kyeong; Jang,Yong  Hyun; Lee,Soyoung; Lee,Sang‑Rae; Choi,Jung  Ho; Park,Jee  Hun; Shin,Tae‑Yong; Kim,Sang‑Hyun

doi:10.3892/mmr.2017.7695

Anti‑inflammatory effect of Amomum xanthioides in a mouse atopic dermatitis model

Authors:
- Young‑Ae Choi
- Jin Kyeong Choi
- Yong Hyun Jang
- Soyoung Lee
- Sang‑Rae Lee
- Jung Ho Choi
- Jee Hun Park
- Tae‑Yong Shin
- Sang‑Hyun Kim
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Affiliations: Department of Pharmacology, Cell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea, Department of Dermatology, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea, Immunoregulatory Materials Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup, Jeollabuk‑do 56212, Republic of Korea, National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongju, Chungcheongbuk‑do 28116, Republic of Korea, R&D Center Pharmaceutical Laboratory, Korean Drug Co., Ltd., Seoul 06300, Republic of Korea, Department of Pharmacy, College of Pharmacy, Woosuk University, Samrye, Jeollabuk‑do 55338, Republic of Korea
Published online on: October 3, 2017 https://doi.org/10.3892/mmr.2017.7695
Pages: 8964-8972

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Abstract

Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disorder. The present study investigated the effects of Amomum xanthioides extract (AXE) on AD‑like skin inflammation using a Dermatophagoides farinae extract (DFE) and 2,4‑dinitrochlorobenzene (DNCB)‑induced mouse AD model. Hematoxylin and eosin staining results demonstrated that repeated DFE/DNCB exposure markedly increased the thickening of the dermis and epidermis, in addition to the infiltration of eosinophils and mast cells. However, oral administration of AXE reduced these histopathological alterations in a dose‑dependent manner. Elevated serum histamine, total and DFE‑specific immunoglobulin E (IgE), and IgG2a were also decreased by treatment with AXE. In addition, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) results demonstrated that the mRNA expression of tumor necrosis factor (TNF)‑α, interferon (IFN)‑γ, interleukin (IL)‑4, IL‑13, IL‑31 and IL‑17A was reduced in ear skin following AXE administration in AD mice. Fluorescence‑activated cell sorting demonstrated that the population of CD4+/IL‑4+, CD4+/IFN‑γ+ and CD4+/IL‑17A+ cells in draining lymph nodes was also significantly decreased in AXE‑treated mice compared with AD mice without AXE treatment. Furthermore, keratinocytes that were stimulated with TNF‑α and IFN‑γ exhibited increased gene expression of pro‑inflammatory cytokines and chemokines, including TNF‑α, IL‑1β, IL‑6, IL‑8, C‑C motif chemokine ligand (CCL)17 and CCL22, as determined by RT‑qPCR. However, upregulation of these genes was reduced by AXE pretreatment. Based on these results, we hypothesize that AXE may be useful in the treatment of allergic skin inflammation, particularly AD.

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