OBJECTIVE： To study the protective mechanism of flavoxate on prostatic hyperplasia in model rats. METHODS： The rats were randomly divided into sham operation group， model group and flavoxate high-dose and low-dose groups （80， 40   mg/kg）， with 8 rats in each group. Except for sham operation group， those groups were emasculated and given sterandryl to induce BPH model. They were given relevant medicine intragastrically 1 h after administration of sterandryl， once a day， for consecutive 4 weeks. Sirius red and Masson staining were used to detect the precipitation of collagen in prostate； immunohistochemistry was used to detect the expressions of prostatic type Ⅰ collagen， FN and E-cadherin； ELISA assay was used to determine the levels of SOD， GPx， MDA， EGF and VEGF in prostate. qPCR assay was used to detect the levels of miR-21 and TGF-β1. RESULTS： Compared with the sham operation group， the prostatic collagen was accumulated； prostatic index， the expression of FN， MDA content and levels of VEGF， EGF， miR-21 and TGF-β1 were increased （P＜0.05）； the expression of E-cadherin， and the activity of SOD and GPx were decreased （P＜0.05）. Compared with model group， the precipitation of prostatic collagen was decreased； prostatic index， the expression of FN， MDA content， the levels of VEGF， EGF， miR-21 and TGF-β1 were decreased in flavoxate high-dose and low-dose groups （P＜0.05）； while the expression of E-cadherin and the activity of SOD and GPx were increased （P＜0.05）. CONCLUSIONS： Flavoxate can inhibit BPH， the mechanism of which may associated with down-regulating the expressions of miR-21 and TGF-β1， inhibiting oxidative stress and angiogenesis and improving epithelial-mesenchymal transition.