title: Ginsenoside Rh2 Suppresses Neovascularization in Xenograft Psoriasis Model.
abstract: OBJECTIVE
  Psoriasis is a common inflammatory skin disease of undetermined etiology and poor prognosis. The current therapies have focused on direct inhibition of local inflammation, e.g. through hormone treatments. However, neovascularization plays a critical role in the development of psoriasis but so far no therapies have been developed to suppress psoriasis-associated neovascularization.
  
  
  METHODS
  We treated AGR129 mice that had received human PN skin grafts with different doses of Ginsenoside Rh2 (GRh2). The acanthosis and papillomatosis index were evaluated. The percentage of T lymphocytes in the grafts was quantified by flow cytometry. The levels of vascularization in the grafts were quantified based on CD31-positive area. We examined the levels of VEGF-A in the skin treated with GRh2. We treated AGR129 mice that had received human PN skin grafts with different doses of soluble Flt-1 (sFlt1) and then evaluated the effects on the acanthosis and papillomatosis index, T lymphocyte percentage and vessel density.
  
  
  RESULTS
  GRh2 dose-dependently decreased the acanthosis and papillomatosis index, T lymphocyte percentage and vessel density in PN skin grafts in mice. GRh2 inhibited VEGF-A levels in the PN skin grafts. Treatment with sFlt1 mimicked the effects of GRh2 on the acanthosis and papillomatosis index, T lymphocyte percentage and vessel density in PN skin grafts in mice.
  
  
  CONCLUSIONS
  GRh2 may have an anti-psoriasis effect through neovascularization suppression.
authors.affiliation: Department of Dermatology, Shanghai Dermatology Hospital, Shanghai, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Zhou
authors.forename: Yunlu
authors.initials: Y
authors.lastname: Gao
authors.forename: Xuemei
authors.initials: X
authors.lastname: Yi
authors.forename: Yangfeng
authors.initials: Y
authors.lastname: Ding
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D015870:Gene Expression; D036145:Ginsenosides / Q000494:pharmacology*; D064593:Heterografts; D006801:Humans; D051379:Mice; D009389:Neovascularization, Pathologic / Q000517:prevention & control*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D011565:Psoriasis / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D012867:Skin / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D013601:T-Lymphocytes; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000494:pharmacology
chemical_list: D004365:Drugs, Chinese Herbal; D036145:Ginsenosides; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A; C055305:ginsenoside Rh2; C501162:FLT1 protein, human; D040281:Vascular Endothelial Growth Factor Receptor-1