Abstract: Objective To investigate the effects of PPARγ ligand rosiglitazone on neointimal hyperplasia and the expression of MMP-2 and TIMP-2 in rat carotid arteries after balloon injure. Methods Treatment group (rosiglitazone 3 mg/kg?d,n=5 ) and control group (saline,n=5) are included in the study. 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 staining. The mRNA levels and protein expression of MMP-2 and TIMP-2 in vascular tissues were measured by RT-PCR and Western-blotting, respectively. Results Both I/M and IA/MA were significantly reduced in rosiglitazone group compared to that in control group at different time points after balloon injury (P＜0.0001). Rosiglitazone markedly suppressed the mRNA and protein expression of MMP-2 in carotid arteries induced by balloon injury（P＜0.0001）. But there were no difference in the mRNA and protein expression of TIMP-2 between rosiglitazone group and control group. Conclusion This study demonstrates that rosiglitazone inhibits neointimal hyperplasia in carotid arteries after balloon injury. Our results suggest that rosiglitazone suppresses neointimal hyperplasia by modulating some taget gene transcription, down regulating MMP-2 expression and breaking the balance of MMP-2 and TIMP-2 in sequence.

Key words: Rosiglitazone, PPARγ, Neointima, MMP-2, TIMP-2