Abstract

Objective: Visfatin is elevated in obesity and T2DM; and thought to be an inflammatory mediator within atherosclerotic lesions inducing gelatinase activity. We investigated the activation of NF-κB a well-known pro-inflammatory transcription factor by visfatin in ECs.

Research Design and Methods: Human ECs were transfected with pNF-κB-Luc plasmid. Using Quantitative PCR, western blot analysis and gelatin zymography, we studied NF-κB signalling in gelatinase mediated vascular inflammation by visfatin; employing the NF-kB inhibitor, BAY 11-7085.

Results: Visfatin significantly increased NF-κB transcriptional activity (P<0.001). Also, we found a significant inhibition of TNFα induced NF-κB activity by visfatin (P<0.001). Furthermore, the NF-κB inhibitor, significantly negated visfatin induced MMP-2/9 mRNA expression, protein levels, and gelatinolytic activity (P<0.001).

Conclusions: Visfatin induced NF-κB signalling in human ECs affects the activation of gelatinases-MMP-2/9, suggesting an important role of visfatin in the pathogenesis of vascular inflammation in obesity and T2DM.