Crocin improves endometriosis by inhibiting cell proliferation and the release of inflammatory factors

Biomed Pharmacother. 2018 Oct:106:1678-1685. doi: 10.1016/j.biopha.2018.07.108. Epub 2018 Jul 29.

Abstract

Endometriosis is one of the most common diseases in women. Inflammation and angiogenesis have been shown to be important in pathogenesis of endometriosis. Crocin is known as an anti-inflammatory, anti- proliferation substance. This study was designed to assess the potential effects of crocin on endometriosis. We established the mice model of endometriosis and administrated crocin to the mice. We monitored the endometriotic lesion growth, PCNA and VEGF expression in the lesion. We tested the serum levels of inflammatory cytokines in crocin-treated endometriosis mice. Finally we tested the effect of crocin on endothelial cell apoptosis and proliferation, and cytokine production in LPS-stimulated human monocyte. Crocin inhibited lesion growth in endometriosis mice and prevented PCNA and VEGF expression in the lesions. Crocin decreased the levels of inflammatory cytokines including INF-γ, TNF-α, VEGF and IL-6 in serum. Crocin inhibited endothelial cells proliferation but did not cause apoptosis in endothelia cells. Crocin inhibited cytokine production in LPS-stimulated THP-1 cells in vitro. Crocin protected endometriosis by inhibiting endothelial cells proliferation and preventing inflammatory cytokines production.

Keywords: Cell proliferation; Crocin; Endometriosis; Inflammatory cytokines; Mice model.

MeSH terms

  • Angiogenesis Inhibitors / pharmacology*
  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Carotenoids / pharmacology*
  • Cell Proliferation / drug effects*
  • Disease Models, Animal
  • Endometriosis / blood
  • Endometriosis / drug therapy*
  • Endometriosis / pathology
  • Endometrium / drug effects*
  • Endometrium / metabolism
  • Endometrium / pathology
  • Female
  • Human Umbilical Vein Endothelial Cells / drug effects
  • Human Umbilical Vein Endothelial Cells / metabolism
  • Humans
  • Inflammation Mediators / blood*
  • Lipopolysaccharides / pharmacology
  • Mice, Inbred BALB C
  • Neovascularization, Pathologic*
  • Proliferating Cell Nuclear Antigen / metabolism
  • THP-1 Cells
  • Time Factors
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Angiogenesis Inhibitors
  • Anti-Inflammatory Agents
  • Inflammation Mediators
  • Lipopolysaccharides
  • Proliferating Cell Nuclear Antigen
  • Vascular Endothelial Growth Factor A
  • vascular endothelial growth factor A, mouse
  • Carotenoids
  • crocin