关键词: NFκB, 双元件诱饵ODN, 球囊损伤, 血管内膜增生, 原代血管平滑肌细胞

Abstract:

[Abstract] Objective  To observe the effects of double-cis-element decoy ODN of nuclear factor-kappa B (NF-κB) on artery intimal hyperplasia in rats and the proliferation of primarily-cultured vascular smooth muscle cells (VSMCs) after arterial balloon injury in rats. Methods  A balloon catheter was introduced through the left external carotid artery to construct intimal injury rat model. The mixture of double-cis-element decoy ODN of p65, a subunit of NF-κB was perfused into the injured vessel as a kind of treatment. The intimal hyperplasia of injured vessel was observed at 3-d and 7-d af? ter operation, respectively. VSMCs were isolated and cultured in vitro and adenovirus, which can express double-cis-element decoy ODN of p65, was introduced to infect primary cells. MTT assay was used to detect the proliferation of treated cells. The high content analysis was used to detect the cell apoptosis. And Western blotting was used to detect expression levels of downstream genes of NF-κB，interleukin-8（IL-8）monocyte chemoa-tracttant protein-1（MCP-1）. Results The intimal hyperplasia after vessel injury was significantly reduced after transfection of double-cis-element decoy ODN of p65 compared with that of treatment of single-cis-element decoy ODN and scrambled control. There were a significantly lower proliferation, a higher apoptosis and lower expression levels of downstream genes of NF-κB in cells treated with double-cis-element decoy ODN of NF-κB. No significant difference was found in down-regulating expression level of MCP-1 between double-cis-element decoy ODN group and single-cis-element decoy ODN group.Conclusion Treatment of double-cis-element decoy ODN of p65, a subunit of NF-κB could inhibit the intimal hyperplasia after injury, which may be caused by inhibition of proliferation of vascular smooth muscle cells.

Key words: NFκB, double-cis-element decoy ODNs of NFκB, balloon injury, neointimal hyperplasia, primary vascular smooth muscle cells