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Objectives: To evaluate the antifibrotic role of captopril during ureteral scarring in a New Zealand rabbit model. Materials and Methods: The tissue expression and the fluctuation of EGF, TGF-β, FN, Col Ia1, Col Ia2 and Col III of the impaired ureter and the contralateral normal ureter were investigated by RT-PCR. The histological changes of the specimens were studied. When the sensitive markers had been selected, 10 New Zealand rabbits were randomly assigned to a captopril group and a control group. The specimens were harvested 2 weeks after the injury and then the histological examination and RT-PCR were performed. Results: By RT-PCR screening, EGF, TGF-β, FN, Col Ia1 and Col Ia2 were found to be significantly related to ureteral scarring (p < 0.05) confirmed by histological examination. The peak level of EGF, TGF-β and Col Ia1 appeared at 2 weeks after the injury, while for Fn and Col Ia2 it was at 3 and 4 weeks after the injury. An obvious reduction of fibrotic scarring was observed in the captopril group. The expression of EGF, Fn and Col Ia2 in the captopril group was significantly lower than in the control group (p < 0.05) after the treatment. Conclusions: EGF, TGF-β, Col Ia1, Col Ia2 and FN seemed to have an important role in the ureteral scarring after injury. Captopril might partially inhibit the fibrotic process by blocking the EGF, Col Ia2 and FN pathway so that it could be a promising treatment after ureteral injury. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]