Astragaloside IV attenuates carotid intimal hyperplasia by suppressing the basic fibroblast growth factor expression in rats

Bacground Percutaneous coronary intervention（PCI） has become one of the most effective treatments in coronary heart disease（CHD）.However,the bottleneck problem of PCI is the in-stent restenosis（ISR）.The aim of this study was to explore the effects of astragaloside IV（AST IV） on suppression of intimal hyperplasia modulation of the expression of basic fibroblast growth factor（b-FGF） in a rat carotid artery balloon injury model.Methods Fifty healthy male Sprague-Dawley（SD）rats were randomly divided into five groups：a sham-operation group（sham）,a model group（model）,and three astragaloside IV-treated groups.Three days before the surgery,1% carboxy methyl cellulose（CMC） or AST IV（20,40 or 60 mg·kg~（- 1）·d~（- 1）） was intragastrically administered into sham or 3 astragaloside-treated groups once a day for 17 days.Hematoxylin-elsin staining was carried out to determine the pathomorphological changes and the neointimal and media area ratio.Immunohistochemistry staining was performed to measure the expressions of proliferating cell nuclear antigen（PCNA）and basic fibrolast growth factor（b-FGF）.PCNA and b-FGF were analyzed with Iamage-Pro Plus.Results（1） The carotid artery intimal hyperplasia in the rats of model was similar to lumen stenosis.Compared with the sham operation group,the area of the new intima and the ratio of the intima to media（I/M） were increased and the lumen area was decreased（P 〈 0.01） in the model group.Astragaloside IV increased the lumen intimal dimension and decreased the area of new intima and the ratio of intima to media in a dose-dependent manner.（2） Compared with the sham-operation group,the expressions of PCNA and b-FGF in carotid artery of model group were significantly increased（P 〈 0.01）.AST IV decreased expressions of PCNA and b-FGF in the carotid artery of rats in a dosedependent manner.Conclusion Astragaloside IV significantly inhibits neointimal hyperplasia of rat carotid artery through down-regulating the expressions of PCNA and b-FGF.