title: Suppression of spontaneous dermatitis in NC/Nga murine model by PG102 isolated from Actinidia arguta.
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.
authors.affiliation: Helixir Co., Ltd, Biotechnology Incubating Center, Seoul National University, Seoul, Korea.
authors.forename: Eun-Jin
authors.initials: EJ
authors.lastname: Park
authors.forename: Kyoung Chul
authors.initials: KC
authors.lastname: Park
authors.forename: Haekwan
authors.initials: H
authors.lastname: Eo
authors.forename: Jangkyun
authors.initials: J
authors.lastname: Seo
authors.forename: Miwon
authors.initials: M
authors.lastname: Son
authors.forename: Kyu Han
authors.initials: KH
authors.lastname: Kim
authors.forename: Yoon-Seok
authors.initials: YS
authors.lastname: Chang
authors.forename: Sang-Heon
authors.initials: SH
authors.lastname: Cho
authors.forename: Kyung-Up
authors.initials: KU
authors.lastname: Min
authors.forename: Mirim
authors.initials: M
authors.lastname: Jin
authors.forename: Sunyoung
authors.initials: S
authors.lastname: Kim
mesh_terms: D029042:Actinidia; D000818:Animals; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D007073:Immunoglobulin E / Q000378:metabolism; D007074:Immunoglobulin G / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D008407:Mast Cells / Q000473:pathology; D051379:Mice; D008815:Mice, Inbred Strains; D008517:Phytotherapy; D010936:Plant Extracts / Q000627:therapeutic use*; D028321:Plant Preparations / Q000627:therapeutic use*; D013154:Spleen / Q000378:metabolism
chemical_list: C515457:Ccl11 protein, mouse; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines; D007074:Immunoglobulin G; C519390:PG102E extract; C519391:PG102T extract; D010936:Plant Extracts; D028321:Plant Preparations; D016753:Interleukin-10; D018664:Interleukin-12; D007073:Immunoglobulin E