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Mediators of Inflammation
Volume 2018 (2018), Article ID 9079527, 11 pages
Research Article

Tabetri™ (Tabebuia avellanedae Ethanol Extract) Ameliorates Atopic Dermatitis Symptoms in Mice

1Department of Genetic Engineering, Sungkyunkwan University, Suwon 16419, Republic of Korea
2Department of Pharmaceutical Engineering, Cheongju University, Cheongju 28503, Republic of Korea
3College of Veterinary Medicine, Chonbuk National University, Iksan 54596, Republic of Korea
4R&I Planning Department, Nutribiotech Co. Ltd., Seoul 06132, Republic of Korea
5Department of Information Statistics, Kangwon National University, Chuncheon 24341, Republic of Korea
6Department of Pharmacy, Sunchon National University, Suncheon 57922, Republic of Korea

Correspondence should be addressed to Young-Jin Son;, Jong-Hoon Kim;, and Jae Youl Cho; ude.ukks@ohceaj

Received 1 October 2017; Accepted 3 January 2018; Published 15 March 2018

Academic Editor: Shin-ichi Yokota

Copyright © 2018 Jae Gwang Park et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Tabebuia avellanedae has been traditionally used as an herbal remedy to alleviate various diseases. However, the plant’s pharmacological activity in allergic and inflammatory diseases and its underlying mechanism are not fully understood. Therefore, we investigated the pharmacological activity of Tabetri (T. avellanedae ethanol extract (Ta-EE)) in the pathogenesis of AD. Its underlying mechanism was explored using an AD mouse model and splenocytes isolated from this model. Ta-EE ameliorated the AD symptoms without any toxicity and protected the skin of 2,4-dinitrochlorobenzene- (DNCB-) induced AD mice from damage and epidermal thickness. Ta-EE reduced the secreted levels of allergic and proinflammatory cytokines, including histamine, immunoglobulin E (IgE), interleukin- (IL-) 4, and interferon-gamma (IFN-γ) in the DNCB-induced AD mice. Ta-EE suppressed the mRNA expression of T helper 2-specific cytokines, IL-4 and IL-5, and the proinflammatory cytokine IFN-γ in the atopic dermatitis skin lesions of AD mice. Moreover, Ta-EE suppressed the mRNA expression of IL-4, IL-5, IFN-γ, and another proinflammatory cytokine, IL-12, in the Con A-stimulated splenocytes. It also suppressed IL-12 and IFN-γ in the LPS-stimulated splenocytes. Taken together, these results suggest that Ta-EE protects against the development of AD through the inhibition of mRNA expression of T helper 2-specific cytokines and other proinflammatory cytokines.