Objective : Benign prostatic hyperplasia(BPH) is one of the most common diseased among elderly men. BPH can be treated with alpha-1 adrenergic blocker or $5{alpha}$-reductase inhibitor(Finasteride) that reduces serum dihydrotestosterone(DHT). Phellodendri Cortex Ex has been broad studied on its chemical components, pharmacological activity, and clinical effects on anti-inflammation, anti-allergy, anti-tumor, immunity, antibacteria and other bioactivities. In this study, we investigated the therapeutic effects and action mechanism of Phellodendri Cortex Ex with a BPH induced by castration and testosterone treatment. Methods : Sprague-Dawley rats were treated with testosterone after castration for induction of experimental benign prostatic hyperplasia, which is similar to human benign prostatic hyperplasia in histopathological profiles. Phellodendri Cortex as an experimental specimen, and Finasteride as a positive control, were administered orally. The prostates were evaluated by histopathological changes, and the expression of $5{alpha}$-reductase genes. Results : While prostates of control rats revealed severe acinar gland atrophy and stromal proliferation, the rats treated with Phellodendri Cortex Ex showed a diminished range of the tissue damage. In the reverse transcription-polymerase chain reaction(RT-PCR) of $5{alpha}$-reductase genes, Phellodendri Cortex inhibited the expression of $5{alpha}$-reductase genes. Conclusions : These findings suggest that Phellodendri Cortex Ex may protect the glandular epithelial cells and also inhibit stromal proliferation in association with the suppression of $5{alpha}$-reductase. From these results, we suggest that Phellodendri Cortex Ex could be a useful agent for treating the benign prostatic hyperplasia.