Role of NF-kB in the Vascular Cell Adhesive Molecular and Neointima Formation

Objective To examine the in vivo effect of NF-kB on ballon-injured vascular cell adhesive molecular-1 (VCAM-1) and vessel proliferation response in the carotid artery of rats. Methods The Sprague-Dawley rats underwent balloon-dilation injury of the left carotid artery. They were divided into 7 groups. Results In model group, sense group and scramble group, the vessel intima area, media area and the intima/media ratio increased after 5d and reached the maximum after 14d. Antisense group, decoy group, antisense plus decoy group improved these observational index ( P 0.05). VCAM-1 mRNA expression were examined 6h after artery injury. The expressions increased continuously after 3,5 and 7d and decreased after 14d. Immunohistochemical studies revealed VCAM-1 protein was maximally positive-stained after 14d. In antisense group, decoy group and antisense plus decoy group, VCAM-1 mRNA expression and protein synthesis decreased in every time point compared with the model group, sense group and scramble group. Western blot studies showed NF-kB p65 was dispersely positive-stained 6h after injury and increased after 1d and reached the peak after 7d, but protein expression was weak after 14d. The antisense group, decoy group and antisense plus decoy group treatment inhibited protein synthesis more significantly than the model group, sense group and scramble group ( P 0.05).Conclusion Nuclear factor NF-kB modulated the gene expression and protein synthesis of VCAM-1. Celluar proliferation in the vessel wall dynamically changes after balloon angioplasty injury. Antisense and decoy oligonucleotide of NF-kB by local lipofectamine transfer inhibit NF-kB activating genes modulatoin, and the combined effect were remarkable than alone.