Ginsenoside Rh2 Suppresses Neovascularization in Xenograft Psoriasis Model

Cell Physiol Biochem. 2015;36(3):980-7. doi: 10.1159/000430272. Epub 2015 Jun 15.

Abstract

Background/aims: 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.

MeSH terms

  • Animals
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Drugs, Chinese Herbal / pharmacology*
  • Gene Expression
  • Ginsenosides / pharmacology*
  • Heterografts
  • Humans
  • Mice
  • Neovascularization, Pathologic / prevention & control*
  • Platelet Endothelial Cell Adhesion Molecule-1 / genetics
  • Platelet Endothelial Cell Adhesion Molecule-1 / metabolism
  • Psoriasis / drug therapy*
  • Psoriasis / genetics
  • Psoriasis / pathology
  • Skin / blood supply
  • Skin / drug effects*
  • Skin / metabolism
  • Skin / pathology
  • T-Lymphocytes
  • Vascular Endothelial Growth Factor A / antagonists & inhibitors
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism
  • Vascular Endothelial Growth Factor Receptor-1 / pharmacology

Substances

  • Drugs, Chinese Herbal
  • Ginsenosides
  • Platelet Endothelial Cell Adhesion Molecule-1
  • Vascular Endothelial Growth Factor A
  • ginsenoside Rh2
  • FLT1 protein, human
  • Vascular Endothelial Growth Factor Receptor-1