Beschreibung:
<jats:p>
<jats:bold>
<jats:italic>Objective—</jats:italic>
</jats:bold>
The activation of nuclear factor-κB (NF-κB) is a crucial step in the arterial wall’s response to injury. The identification and characterization of the NF-κB essential modulator–binding domain (NBD) peptide, which can block the activation of the IκB kinase complex, have provided an opportunity to selectively abrogate the inflammation-induced activation of NF-κB. The aim of the present study was to evaluate the effect of the NBD peptide on neointimal formation.
</jats:p>
<jats:p>
<jats:bold>
<jats:italic>Methods and Results—</jats:italic>
</jats:bold>
In the rat carotid artery balloon angioplasty model, local treatment with the NBD peptide (300 μg/site) significantly reduced the number of proliferating cells at day 7 (by 40%;
<jats:italic>P</jats:italic>
<0.01) and reduced injury-induced neointimal formation (by 50%;
<jats:italic>P</jats:italic>
<0.01) at day 14. These effects were associated with a significant reduction of NF-κB activation and monocyte chemotactic protein-1 expression in the carotid arteries of rats treated with the peptide. In addition, the NBD peptide (0.01 to 1 μmol/L) reduced rat smooth muscle cell proliferation, migration, and invasion in vitro. Similar results were observed in apolipoprotein E
<jats:sup>−/−</jats:sup>
mice in which the NBD peptide (150 μg/site) reduced wire-induced neointimal formation at day 28 (by 47%;
<jats:italic>P</jats:italic>
<0.01).
</jats:p>
<jats:p>
<jats:bold>
<jats:italic>Conclusion—</jats:italic>
</jats:bold>
The NBD peptide reduces neointimal formation and smooth muscle cell proliferation/migration, both effects associated with the inhibition of NF-κB activation.
</jats:p>