Insulin inhibits NFκB and MCP-1 expression in human aortic endothelial cells

In view of our recent demonstration that insulin inhibits the expression of intercellular adhesion molecule-1 (ICAM-1) and the fact that ICAM-1 expression is known to be modulated by nuclear factor-kappaB (NF kappaB), We have now investigated whether insulin inhibits intranuclear NF kappaB binding activity. We have also investigated whether insulin inhibits the pro-inflammatory chemokine, monocyte chemoattractant protein-1 (MCP-1), which attracts leucocytes to the inflamed sites and is also regulated by NF kappaB. insulin was incubated with cultured human aortic endothelial cells (HAEC) at 0, 100 and 1000 muU/mL. Intranuclear NF kappaB binding activity was suppressed by approximately 45 % at 100 muU/mL and by 60 % at 1000 muU/mL (p<0.05). MCP-1 mRNA expression was also suppressed by 47% at 100 <mu>U/mL and by 79 % at 1000 muU/mL (p<0.05). We conclude that insulin at physiologically relevant concentrations exerts an inhibitory effect on the cardinal pro-inflammatory transcription factor NF<kappa>B and the pro-inflammatory chemokine MCP-1; these effects suggest an anti-inflammatory and potential anti-atherogenic affects of insulin.