Objective:To investigate the effect of PPARγ ligand rosiglitazone on neointimal hyperplasia and the expression of c-Fos and p27kip1 in rat carotid arteries after balloon injure.Methods:Vascular restenosis in rat carotid arteries was established by balloon denudation.The thickness and area ratios of intima to media(I/M and IA/MA) were measured by using hematoxylin and eosin stain at different time after balloon injury.The mRNA levels and protein expression of c-Fos and p27kip1 in vascular tissues were measured by RT-PCR and Western blot

respectively.Results:Both I/M and IA/MA were significantly reduced in rosiglitazone treatment group [3 mg/(kg·d)] compared to that in control group treated with saline [3 mg/(kg·d)](P<0.000 1

n=5).Although barely detectable in normal arteries

the mRNA and protein expression of c-Fos were increased one day after balloon injury.The increases of c-Fos reached peak levels on day 7 and declined after 14 days.Rosiglitazone markedly suppressed the mRNA and protein expression of c-Fos in arteries induced by balloon injury.In contrast to c-Fos

the expression of p27kip1 in arteries was decreased after balloon injury.The lowest level of p27kip1 were seen on day 7 after balloon injury and gradually recovered from day 14.The mRNA and protein expression of p27kip1 were significantly increased in rosiglitazone treatment group compared that in control group.Conclusion:These studies demonstrate that rosiglitazone inhibit neointimal hyperplasia in carotid arteries after balloon injury.Our results suggest that rosiglitazone suppresses neointimal hyperplasia by modulating c-Fos and p27kip1 expression.