Effects of Plant Sphingolipids on Inflammatory Stress in Differentiated Caco-2 Cells

J Oleo Sci. 2017;66(12):1337-1342. doi: 10.5650/jos.ess17171.

Abstract

To determine the mechanism underlying the anti-inflammatory effects of plant sphingolipids, especially plant glucosylceramide (GlcCer), the effects of plant sphingolipids on inflammatory stress in differentiated Caco-2 cells were compared to those of a sphingolipid of animal origin, galactosylceramide (GalCer). Addition of GlcCer or GalCer suppressed cell injury caused lipopolysaccharide (LPS)- and TNF-α-induced inflammatory stress and induction of apoptosis in differentiated Caco-2 cells. There was no difference in the suppressive effect between GlcCer and GalCer. The inflammatory cytokines and chemokines induced by LPS were suppressed by GlcCer. GlcCer remained on the cell surface. The results of this study can be summarized as follows: 1) sphingolipids such as GlcCer have potent anti-inflammatory effects; 2) GlcCer suppresses LPS-induced production of cytokines and apoptosis; 3) sphingolipids may remain on the surface of cells, and 4) the chemical properties of sphingolipids may prevent the interaction between LPS and its receptor.

Keywords: colon inflammation; cytokine; glycosylceramide; sphingolipid.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Anti-Inflammatory Agents*
  • Apoptosis / drug effects
  • Caco-2 Cells
  • Cell Differentiation
  • Cytokines / metabolism
  • Galactosylceramides / pharmacology*
  • Glucosylceramides / pharmacology*
  • Humans
  • Inflammation Mediators / metabolism
  • Lipopolysaccharide Receptors / metabolism
  • Lipopolysaccharides / adverse effects
  • Lipopolysaccharides / metabolism
  • Plants / chemistry*
  • Sphingolipids / pharmacology*
  • Tumor Necrosis Factor-alpha / adverse effects

Substances

  • Anti-Inflammatory Agents
  • Cytokines
  • Galactosylceramides
  • Glucosylceramides
  • Inflammation Mediators
  • Lipopolysaccharide Receptors
  • Lipopolysaccharides
  • Sphingolipids
  • Tumor Necrosis Factor-alpha