Omentin plays an anti-inflammatory role through inhibition of TNF-α-induced superoxide production in vascular smooth muscle cells

Eur J Pharmacol. 2012 Jul 5;686(1-3):116-23. doi: 10.1016/j.ejphar.2012.04.033. Epub 2012 Apr 24.


Omentin is a recently identified adipocytokine and its effect in vasculature is largely unknown. Here we examined the effects of omentin on smooth muscle cells (SMCs) inflammatory states. Western blotting was performed to analyze inflammatory signal transduction in cultured SMCs. Phosphorylation of nuclear factor-κB (NF-κB), p38 and JNK, and expression of vascular cell adhesion molecule (VCAM)-1 and cyclooxygenase-2 were not induced by omentin (50-300ng/ml, 20min or 24h). On the other hand, tumor necrosis factor-α (TNF-α; 10ng/ml, 20min)-induced phosphorylation of p38 and JNK was significantly inhibited by omentin pretreatment in a concentration-dependent manner (50-300ng/ml, 30min). TNF-α (24h)-induced expression of VCAM-1 was also significantly inhibited by omentin pretreatment in a concentration-dependent manner. Both inhibitor of p38 (SB203580) and JNK (SP600125) significantly inhibited TNF-α-induced VCAM-1 expression. Omentin (300ng/ml, 30min) inhibited TNF-α (1h)-induced nicotinamide adenine dinucleotide phosphate oxidase activity as determined by lucigenin assay. An antioxidant drug, N-acetyl-l-cysteine significantly inhibited TNF-α-induced phosphorylation of p38 and JNK. Furthermore, omentin (300ng/ml, 30min) significantly inhibited TNF-α (24h)-induced monocytic cells adhesion to SMCs. In rat isolated thoracic aorta, omentin (300ng/ml, 30min) inhibited TNF-α (24h)-induced VCAM-1 expression. The present results demonstrate for the first time that omentin plays an anti-inflammatory role by preventing the TNF-α-induced VCAM-1 expression in SMCs. It is suggested that omentin inhibits TNF-α-induced VCAM-1 expression via preventing the activation of p38 and JNK at least in part through inhibition of superoxide production.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Aorta, Thoracic / drug effects
  • Aorta, Thoracic / physiology
  • Cell Adhesion / drug effects
  • Cytokines / pharmacology*
  • GPI-Linked Proteins / pharmacology
  • Humans
  • In Vitro Techniques
  • JNK Mitogen-Activated Protein Kinases / immunology
  • Lectins / pharmacology*
  • Male
  • Monocytes / drug effects
  • Monocytes / physiology
  • Muscle, Smooth, Vascular / drug effects*
  • Muscle, Smooth, Vascular / physiology
  • Rats
  • Rats, Wistar
  • Recombinant Proteins / pharmacology
  • Superoxides / immunology*
  • Tumor Necrosis Factor-alpha / immunology*
  • Tumor Necrosis Factor-alpha / pharmacology
  • U937 Cells
  • Vascular Cell Adhesion Molecule-1 / immunology
  • p38 Mitogen-Activated Protein Kinases / immunology


  • Anti-Inflammatory Agents
  • Cytokines
  • GPI-Linked Proteins
  • ITLN1 protein, human
  • Lectins
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Superoxides
  • JNK Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases