1. ¹Helixir Co., Ltd, Biotechnology Incubating Center, Seoul National University, Seoul, Korea
2. ²Department of Biological Sciences and Institute of Molecular Biology and Genetics, Seoul National University, Seoul, Korea
3. ³Dong-A Co., Ltd, R&D Center, Youngin, Gyeonggi-do, Korea
4. ⁴Department of Dermatology, Seoul National University Hospital, Seoul, Korea
5. ⁵Department of Allergy, Seoul National University Hospital, Seoul, Korea
6. ⁶College of Oriental Medicine, Daejeon University, Daejeon, Korea

Correspondence: Dr Sunyoung Kim, Department of Biological Sciences, Institute for Molecular Biology and Genetics, Seoul National University, San 56-1, Shillim-dong, Gwanak-gu, Seoul 151-742, Korea. E-mail: sunyoung@plaza.snu.ac.kr

Received 31 March 2006; Revised 21 September 2006; Accepted 16 October 2006; Published online 28 December 2006.

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease, which requires safe and effective pharmacological therapy. We previously found that two preparations from Actinidia arguta, PG102T, and PG102E, could modulate Th1/Th2 pathways and suppress IgE biosynthesis. This study was performed to assess the therapeutic effects of PG102T and PG102E on the development of dermatitis in NC/Nga mice, characterized by the spontaneous onset of AD along with an elevated level of IgE under conventional conditions. PG102T or PG102E administration significantly reduced dermatitis severity as well as scratching tendency in conventional mice. The suppression of dermatitis by PG102 was accompanied by a decrease in the plasma level of IgE, IgG1, and IL-4 and also by an increase in that of IgG2a and IL-12. The splenic level of IL-4, IL-5, and IL-10 was downregulated, whereas that of IFN- and IL-12 was increased. The number of eosinophils and the expression of eotaxin and thymus and activation-regulated chemokine were decreased by PG102T or PG102E. Histological findings also indicated that the thickening of epidermis/dermis and the dermal infiltration of inflammatory cells including mast cells were greatly inhibited. These data suggest that PG102 may be effective therapeutic agents for the treatment of AD.