Eriochloa villosa Alleviates Progression of Benign Prostatic Hyperplasia in vitro and in vivo

• Published in: Research and reports in urology 2022-01, Vol.14, p.313-326
• Main Authors: Baek, Eun Bok, Hwang, Youn-Hwan, Park, Suyoung, Hong, Eun-Ju, Won, Young-Suk, Kwun, Hyo-Jung
• Format: Article
• Language: English
• Subjects: Acids; Androgen receptors; Antibodies; Antigens; Antioxidants; Apoptosis; Bcl-2 protein; benign prostatic hyperplasia; Catalase; Cell cycle; Cell proliferation; Cyclooxygenase-2; Dihydrotestosterone; Eriochloa villosa; Genital diseases; Hyperplasia; Inflammation; Injection; Interleukin 8; Laboratory animals; Original Research; Oxidative stress; Proliferating cell nuclear antigen; proliferation; Prostate; Prostate cancer; Prostate-specific antigen; Proteins; Serum levels; Testosterone
• ISSN: 2253-2447; 2253-2447
• DOI: 10.2147/RRU.S381713

Introduction: Benign prostatic hyperplasia (BPH) is a non-neoplastic proliferative disease of the prostate. Eriochloa villosa (EV) reportedly possesses various pharmacological activities, including anti-lipase activity and modulation of various antioxidative enzymes. In this study, we investigate the therapeutic potential of EV against BPH in a testosterone-induced BPH rat model. Methods: Rats were subjected to a daily subcutaneous injection of testosterone (3 mg kg− 1) for 4 weeks to induce BPH. Along with testosterone, rats in the treatment group were administered finasteride (10 mg kg− 1) or EV (150 mg kg− 1) via oral gavage. Prostatic cancer (LNCaP) cell line was used to examine the effect of EV. Results: Finasteride and EV significantly decrease the relative prostate weight, serum levels of dihydrotestosterone and testosterone, and prostate epithelial thickness. Testosterone injection induced prostatic hyperplasia and proliferating cell nuclear antigen expression; however, EV treatment significantly attenuated these effects. Moreover, finasteride- and EV-treated rats exhibit an increase in the number of TUNEL-positive cells and reduced Bcl-2 expression in the prostate tissues compared with the testosterone-treated animals. Furthermore, EV suppresses inflammatory cytokines, including interleukin (IL)-6 and IL-8, in the prostate tissues. Meanwhile, the expression of inflammatory mediator cyclooxygenase-2 is consistently upregulated in testosterone-treated rats, whereas EV treatment significantly reverses this effect. Notably, EV treatment suppresses malondialdehyde (MDA) levels and upregulates testosterone-induced catalase (CAT) expression. In addition, EV suppresses expression of androgen receptor (AR) and prostate-specific antigen (PSA) induced by testosterone in LNCaP cells. Conclusion: The present study results suggest that EV regulates prostatic proliferation, apoptosis, response to inflammation, and oxidative stress in the BPH rat model, and may, therefore, serve as a useful therapeutic agent for BPH.