Bortezomib reduces neointimal hyperplasia in a rat carotid artery injury model.

ABSTRACT:

Background and objectives

The ubiquitin-proteasome system is the major intracellular protein degradation pathway in the eukaryotic cells. Bortezomib inhibits 26S proteasome-induced I-κBα degradation and suppresses nuclear factor-kappa B (NF-κB) activation. We examined the effect of bortezomib on neointima formation after of a rat carotid artery balloon injury.

Materials and methods

After carotid artery balloon denudation, bortezomib was immediately administered by tail vein injection (systemic treatment) and by using an F-127 pluronic gel (perivascular treatment). Two weeks after the injury, we compared the degree of neointima formation in the carotid artery and the tissue expression patterns of NF-κB and I-κBα.

Results

The systemic treatment group exhibited a 29% red

SUBMITTER: Kim KS 

PROVIDER: S-EPMC3808854 | biostudies-literature | 2013 Sep

REPOSITORIES: biostudies-literature