Atorvastatin Antagonizes The Visfatin-Induced Expression Of Inflammatory Mediators Via The Upregulation Of Nf-Kappa B Activation In Hcaecs

The present study investigated whether atorvastatin antagonizes the visfatin-induced expression of inflammatory mediators in human coronary artery endothelial cells (HCAECs). Several analysis methods, such as reverse transcription-quantitative polymerase chain reaction, western blot analysis and H2DCFDA incubation, were used in the present study. The data showed that atorvastatin decreased the visfatin-induced expression of interleukin (IL)-6 and IL-8 in HCAECs. In addition, atorvastatin inhibited the visfatin-induced expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in HCAECs. In addition, the present study found that atorvastatin inhibited the visfatin-activated nuclear factor-kappa B (NF-kappa B) signal pathway by preventing extracellular signal-regulated kinase phosphorylation in HCAECs. Atorvastatin significantly inhibited visfatin-induced NF-kappa B activity via the upregulation of reactive oxygen species production. Atorvastatin, a visfatin antagonist (FK866) and an NF-kappa B inhibitor (BAY11-7082) decreased the visfatin-induced expression of inflammatory mediators via the upregulation of NF-kappa B activation in HCAECs. These results suggest that atorvastatin may inhibit the visfatin-induced upregulation of inflammatory mediators through blocking the NF-kappa B signal pathway. The findings of the present study provide a potential use for atorvastatin and visfatin in the pathogenesis of HCAEC dysfunction. This knowledge may contribute to the development of novel therapies for atherosclerosis.