# Calamagrostis arundinacea Extract Mitigates Testosterone Induced Prostatic Hyperplasia in Rats

## TL;DR

This study shows that Calamagrostis arundinacea extract reduces prostate enlargement in rats caused by testosterone, offering a potential natural treatment for BPH.

## Contribution

The study demonstrates the anti-hyperplastic effects of Calamagrostis arundinacea extract in a testosterone-induced BPH rat model.

## Key findings

- CA extract significantly reduced prostate weight and testosterone/DHT levels in TP-treated rats.
- CA suppressed epithelial thickening and hyperplastic changes while increasing apoptosis in prostate tissue.
- CA inhibited PI3K/Akt/mTOR signaling and downregulated genes like Igf-2, Tgf-β, and Vegf.

## Abstract

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.