Inhibition of Neointimal Hyperplasia Development by MCI-186 is Correlated With Downregulation of Nuclear Factor-_κB Pathway

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Background Atherosclerosis is a progressing inflammatory response mediated by various signaling molecules among which nuclear factor _kB (NF-_κB) is thought to have a pivotal role. This study demonstrated the efficacy of antioxidant MCI-186 in preventing the progression of atherosclerosis by inhibiting signaling molecules such as NF-_κB. Methods and Results Balloon injury of intima was performed in the right common carotid artery of Japanese male white rabbits, which were then fed a 1% high cholesterol diet for 4 weeks, after assigning them to either the control (n=7) or MCI-186 (0.5mg・kg^<-1>・day^<-1>, n=7) group. Histological analysis revealed a reduction in neointimal thickness and lipid deposition in the subendothelial area of the MCI-186 group. Immunohistochernical analysis revealed attenuation of E-selectin expression, macrophage migration and proliferation of smooth muscle cells in the MCI-186 treated group. In in vitro studies, rabbit aorta smooth muscle cells were incubated with rIL-1β in either the presence or absence of MCI-186. MCI-186 significantly inhibited rIL-1β-induced proliferation of smooth muscle cells from rabbit aorta, as well as the activation of NF-_κB. Moreover, western blot analysis showed the inhibitory action of MCI-186 on the nuclear translocation of NF-_κB in human umbilical vein endo-thelial cells under rIL-1β stimulation. Conclusions MCI-186 could provide a novel therapeutic strategy for atherosclerosis by inhibiting the NF-_κB pathway.
社団法人日本循環器学会の論文
2008-04-20

Inhibition of Neointimal Hyperplasia Development by MCI-186 is Correlated With Downregulation of Nuclear Factor-_κB Pathway

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