초록
Objective : In benign prostatic hyperplasia, dihydrotestosterone acts as a potent cellular androgen and promotes prostate growth. Inhibiting enzyme $5{\alpha}$-reductase that is involved in the conversion of testosterone to the active form dihydrotestosterone reduces this excessive prostate growth. The mechanism on benign prostatic hyperplasia is substantiating evidence to support the clinical value in the evaluation of therapeutic efficacy. In this study, we investigated the effects of Lygodium japonicum on cyto-pathological alterations and expression of $5{\alpha}$-reductase in the rat model of benign prostatic hyperplasia 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. Lygodium japonicum as an experimental specimen, and finasteride as a positive control, were administered orally. The prostates were evaluated by histopathological changes and testosterone levels. Also, the prostates were observed by hematological alterations of AST, ALT, ${\gamma}$-GTP, BUN and creatinine. Results : The rats treated with Lygodium japonicum showed a diminished range of luminal cell and duct epithelial cell damage. The stromal elements and connective tissue proliferation of Lygodium japonicum treated group as compared to the control group decreased. Conclusions : These findings suggest that Lygodium japonicum may protect the glandular epithelial cells. We concluded that Lygodium japonicum could be a useful remedy agent for treating the benign prostatic hyperplasia.
