Background: Benign prostatic hyperplasia (BPH) is an age-associated urological condition defined by abnormal multiplication of both stromal and epithelial components within the prostate. Calamagrostis arundinacea (CA), a species of perennial grass native to East Asia, has been recognized for its anti-inflammatory and antioxidant biological activities. The present study examined whether CA extract could attenuate prostatic enlargement induced by testosterone propionate (TP) in rats. Methodology: To establish the experimental model, rats received subcutaneous TP injections (3 mg/kg/day) for four consecutive weeks. During the same period, an extract of CA (150 mg/kg/day) was orally administered. Results: TP-treated animals developed significant prostatic enlargement, whereas CA supplementation markedly reduced prostate weight and significantly decreased circulating dihydrotestosterone (DHT) and testosterone levels. Microscopic analysis demonstrated that CA mitigated glandular epithelial thickening and suppressed hyperplastic alterations. In addition, CA reduced proliferating cell nuclear antigen (PCNA) expression and increased apoptotic cell numbers, as evidenced by TUNEL staining. Gene expression analysis further revealed significant downregulation of insulin-like growth factor-2 (Igf-2), transforming growth factor-β (Tgf-β), and vascular endothelial growth factor (Vegf), in CA-treated prostates. Moreover, CA inhibited activation of the PI3K/Akt/mTOR signaling cascades by reducing phosphorylation of Akt and mTOR. Conclusions: Overall, these results indicate that CA extract alleviates testosterone-induced BPH through suppression of growth-related signaling cascades and induction of apoptosis, suggesting its potent value as a phytotherapeutic strategy for BPH management.

BACKGROUND/OBJECTIVES: L. (PV), a perennial herbaceous plant native to Europe and Asia, has anti-inflammatory, antioxidant, and antimicrobial effects. In this study, we determined the effect of PV extract on the development of BPH. METHODS: Rats were treated via a daily hypodermic injection of testosterone propionate (TP; 3 mg/kg) for 4 weeks. Groups of BPH rats were treated with or without PV (60 or 80 mg/kg) by oral gavage. RESULTS: In BPH model rats, PV considerably reduced their relative prostate weight and serum concentrations of dihydrotestosterone (DHT) and testosterone. The TP-induced increases in epithelial thickness in the prostate, proliferating cell nuclear antigen (PCNA) expression, and cyclin D1 expression were remarkably reduced, whereas terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL)-positive cells and cleaved caspase-3 levels were increased, in PV-treated rats compared to BPH rats. The mRNA expression levels of growth factors, such as transforming growth factor-β (TGF-β), fibroblast growth factor (FGF), and insulin-like growth factor (IGF-2), were significantly reduced in PV-treated rats. Mechanistically, the TP-induced activation of c-Jun N-terminal kinase (JNK) was reduced by PV administration. CONCLUSIONS: These results designate that PV effectively ameliorates the development of testosterone-induced BPH through anti-androgenic, anti-proliferative, and pro-apoptotic activities, suggesting that it could be a potential therapeutic substance for BPH.