Effect Of Cyclooxygenase-2and Its Selective Injury Inhibitors On Neointimal Proliferation After Balloon In Rat Carotid Artery

Objective To discuss the possible mechanism of endometrial hyperplasia and vascular restenosis with observing the dynamic change of COX-2, PGE2and VEGF which are expressed after the damages that have been made in rat’s sacculus and celecoxib that has been delivered.Methods Sixty SD male rats were divided into three groups at random which included negative control group (A group), positive control group (B group) and drug delivering group (C group). Each group was to be further split into four subunits which consisted of6h,7d,14d and28d. Using fluorescent quantitation PCR to detect the expressions of COX-2and PGE2mRNA in tissues. Using ELISA to test the expression of VEGF in blood. Utilizing carotid artery and the pathological images of vascular tissue to analyze the variation of intima forms.Results The subunits in group A neither showed any obvious changes of factors of detecting data nor significant changes of images of tissue. All factors in group B started to increase after they had expressed for6h. All factors reached the peak expression14d. These factors still expressed highly when expressed28d. The subunits of B group was distinctly different from the corresponding expressions of group A (P<0.05). All figures of factors in the subunits of group C were lower than that of the subunits of group B. All figures of factors in the subunits of group C were higher than that of the subunits of group A (P<0.05). Images of tissue in subunit of every group showed the intima hyperplasia had the same tendency with the expressions of all factors above.Conclusion Celecoxib can restrain the hyperplasia of endothelial cell by inhibiting COX-2of expression in injured vessel, that probably provides a new way to the prevention of postoperative restenosis. The mechanism’s operation above is that Celecoxib causes the chain reaction of expression’s decrease among COX-2, PGE2and VEGF. The decrease of VEGF results in weakening the hyperplasia of endothelial cell.