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Suppression of spontaneous dermatitis in NC/Nga murine model by PG102 isolated from Actinidia arguta

Cited 41 time in Web of Science Cited 48 time in Scopus
Authors
Park, Eun-Jin; Park, Kyoung Chul; Eo, Haekwan; Seo, Jangkyun; Son, Miwon; Kim, Kyu Han; Chang, Yoon-Seok; Cho, Sang-Heon; Min, Kyung-Up; Jin, Mirim; Kim, Sunyoung
Issue Date
2006
Publisher
Nature Publishing Group
Citation
J Invest Dermatol 127:1154-60
Keywords
*ActinidiaAnimalsChemokine CCL11Chemokines, CC/metabolismCytokines/metabolismDermatitis, Atopic/*drug therapy/metabolism/pathologyDisease Models, AnimalFemaleImmunoglobulin E/metabolismImmunoglobulin G/metabolismInterleukin-10/metabolismInterleukin-12/metabolismMast Cells/pathologyMiceMice, Inbred Strains*PhytotherapyPlant Extracts/*therapeutic usePlant Preparations/*therapeutic useSpleen/metabolism
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-gamma 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.
ISSN
1523-1747 (Electronic)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17195015

http://hdl.handle.net/10371/24902
DOI
https://doi.org/10.1038/sj.jid.5700658
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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