Aim To study the expression of aldose reductase(AR) in the carotids of the rats with restenosis in order to probe into the relationship between AR expression and intimal hyperplasia,and further explore the inhibition of atorvastatin on AR expression and intimal hyperplasia in the carotids with restenosis. Methods 24 healthy male SD rats were divided into the injuried group without treatment,the fake operation group and the atorvastatin group by chance.Each group had 8 rats.The right carotids were injuried by air-drying operation in the treatment group and the group with operation but without treatment.The left carotids were acted as the controls.The rats were killed after 7 days and 14 days respectively.Dying with HE to examine the intimal and the medial layers' proliferation.And the acreage of the intimal and the medial layers and their ratio were calculated as well.Then the expression of nuclear factor-κB(NF-κB) and AR were examined by immunohistochemical methods and FISH in situ hybridization. Results Seven days after the injury,the intimal hyperplasia could be seen obviously in the injuried sides of the carotids,by the end of 14 days,the intimal hyperplasia aggravated.While the carotids in the control sides were not.The acreage of the intimal layers,the ratio of the intimal and the medial layers in the atorvastatin group was obviously lower than that of the operation group without treatment.The difference was obvious when compared with each other(p<0.05 or p<(0.01)).The expression of AR and NF-κB in the injuried sides was obviously higher than that of the control sides.The expression of AR and NF-κB in the atorvastatin group was obviously lower than that of the untreatment group.Compared with each other,the difference was obvious(p<0.05 or p<0.01). Conclusion AR may be concerned with the neointima and the form of restenosis in the injuried carotids of the rats.Atorvastatin could obviously inhibit the neointima and the form of the restenosis.Atorvastatin might inhibit vascular smooth muscle cells(VSMC) proliferation through inhibiting AR and NF-κB expression.