Suppressive effects of pelargonidin on lipopolysaccharide-induced inflammatory responses

Chem Biol Interact. 2019 Apr 1:302:67-73. doi: 10.1016/j.cbi.2019.02.007. Epub 2019 Feb 10.

Abstract

Pelargonidin (PEL) is a well-known red pigment found in plants, and has been reported as having important biological activities that are potentially beneficial for human health. Here, we tested the possible use of PEL in the treatment of lipopolysaccharide (LPS)-mediated vascular inflammatory responses. The anti-inflammatory activities of PEL were determined by measuring permeability, neutrophils adhesion and migration, and activation of pro-inflammatory proteins in LPS-activated human umbilical vein endothelial cells (HUVECs) and mice. We found that PEL inhibited LPS-induced barrier disruption, expression of cell adhesion molecules (CAMs), and adhesion/transendothelial migration of neutrophils to human endothelial cells. PEL also suppressed LPS-induced hyperpermeability and leukocytes migration in vivo. Furthermore, PEL suppressed the production of tumor necrosis factor-α (TNF-α) or Interleukin (IL)-6 and the activation of nuclear factor-κB (NF-κB) or extracellular regulated kinases (ERK) 1/2 by LPS. Moreover, treatment with PEL resulted in reduced LPS-induced lethal endotoxemia. These results suggest that PEL possesses anti-inflammatory functions by inhibiting hyperpermeability, expression of CAMs, and adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapy for vascular inflammatory diseases.

Keywords: Barrier integrity; Inflammation; Lipopolysaccharide; Pelargonidin.

MeSH terms

  • Animals
  • Anthocyanins / pharmacology*
  • Anthocyanins / therapeutic use
  • Anti-Inflammatory Agents / pharmacology*
  • Anti-Inflammatory Agents / therapeutic use
  • Cell Adhesion / drug effects*
  • Cell Adhesion Molecules / metabolism
  • Cell Movement / drug effects
  • Endotoxemia / drug therapy
  • Endotoxemia / pathology
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Interleukin-6 / metabolism
  • Leukocytes / cytology
  • Leukocytes / drug effects
  • Leukocytes / metabolism
  • Lipopolysaccharides / toxicity*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • NF-kappa B / metabolism
  • Permeability / drug effects
  • Toll-Like Receptor 4 / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Anthocyanins
  • Anti-Inflammatory Agents
  • Cell Adhesion Molecules
  • Interleukin-6
  • Lipopolysaccharides
  • NF-kappa B
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • pelargonidin
  • p38 Mitogen-Activated Protein Kinases