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Evidence-Based Complementary and Alternative Medicine
Volume 5 (2008), Issue 2, Pages 173-180
Original Article

Sopungyangjae-Tang Inhibits Development of Dermatitis in Nc/Nga Mice

1BK21 Project Team, College of Pharmacy, Chosun University, Seosuk-dong, Dong-gu, Gwangju 501-759, Republic of Korea
2Department of Pathology, College of Medicine, Chosun University, Seosuk-dong, Dong-gu, Gwangju 501-759, Republic of Korea
3Department of Prescription, College of Oriental Medicine, Daegu Haany University, Daegu 706-060, Republic of Korea
4College of Biomedical Laboratory Science, Konyang University, Daejeon, Republic of Korea

Received 3 July 2006; Accepted 16 January 2007

Copyright © 2008 Yuba Raj Pokharel 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.


Sopungyangjae-Tang (SYT) is a traditional Korean decoction used for the treatment of dermatitis. The aim of this study was to confirm whether or not SYT has a preventive effect on the development of atopic dermatitis in dinitrochlorobenzene-applied Nc/Nga mice. SYT was administered orally to Nc/Nga mice, which led to the remarkable suppression of the development of dermatitis, as determined by a histological examination and the serum IgE levels. Moreover, SYT inhibited the production of thymus- and activation-regulated chemokine (TARC) and its mRNA expression in a keratinocyte cell line, HaCaT, which had been stimulated with tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). Activation of the nuclear factor-κB (NF-κB) or activator protein-1 (AP-1) is one of the key steps in the signaling pathways mediating induction of TARC. In this study, SYT selectively suppressed NF-κB activation, which may be essential for TARC expression in TNF-α/IFN-γ treated keratinocytes. The inhibitory effect of SYT on NF-κB activation and TARC production might be associated with the anti-dermatitic effects of SYT.