| Objective: To investigate the effects of atorvastatin on the expression of Nur77 in vas cular smooth muscle cells (VSMCs ) of rat carotid artery postangioplasty restenosis models which were established , and to explore the relationship between Nur77 and VSMCs proliferation and new mechanism which atorvastatin prevented restenosis of blood vessel after balloon-injury.Methods: 120 clean-class male Sprague Dawley rats (weight 300-350g) were randomly divided into three groups. Labeled: blank control group (sham-operated group ) (BCG) 10 rats, control group (carotid artery balloon- injury group ) (CG) 55 rats, and carotid artery balloon- injury + atorvastatin intervention group (AIG) 55 rats. The arteries were harvested on day 7, 14, 21, 28 after balloon-injury. Analysis and comparison the ratio of intima to media thickness and lumen area were assessed by pathomorphology.β-SMA,Nur77 and PCNA expression were assessed by immunohistochemistry; PDGF-B,Nur77,ERK,NF-κB expression were assessed by real-time PCR (RT-PCR); Nur77 expression was assessed by Western Blot. Result: Nur77 expression levels and the ratios of intima to media thickness and lumen area of carotid artery balloon- injury group were higher compared with blank control group (BCG); Nur77 expression levels and the ratio of intima to media thickness and lumen area of carotid artery balloon- injury + atorvastatin intervention group (AIG) were lower compared with control group (CG).Conclusion: After carotid artery balloon-injury in rats, compared with before it , thickness of intima of carotid artery were higher, Nur77 expression levels of vascular smooth muscle were higher, and proliferation of VSMCs were significantly almost at the same time . Atorvastatin inhibited VSMCs proliferation by regulating nuclear orphan receptor nur77 expression. By reducing the Nur77 expression in VSMCs proliferation, statins prevented new vascular damage mechanism of postoperative restenosis. |
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