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Eriochloa villosa Alleviates Progression of Benign Prostatic Hyperplasia in vitro and in vivo.
Baek, Eun Bok; Hwang, Youn-Hwan; Park, Suyoung; Hong, Eun-Ju; Won, Young-Suk; Kwun, Hyo-Jung.
Affiliation
  • Baek EB; Department of Veterinary Pathology, College of Veterinary Medicine, Chungnam National University, Daejeon, Korea.
  • Hwang YH; Herbal Medicine Research Division, Korean Institute of Oriental Medicine, Daejeon, Korea.
  • Park S; Department of Veterinary Pathology, College of Veterinary Medicine, Chungnam National University, Daejeon, Korea.
  • Hong EJ; Department of Veterinary Pathology, College of Veterinary Medicine, Chungnam National University, Daejeon, Korea.
  • Won YS; Laboratory Animal Resource Center, Korean Research Institute of Bioscience and Biotechnology, Chungbuk, Korea.
  • Kwun HJ; Department of Veterinary Pathology, College of Veterinary Medicine, Chungnam National University, Daejeon, Korea.
Res Rep Urol ; 14: 313-326, 2022.
Article in En | MEDLINE | ID: mdl-36187165
ABSTRACT

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.
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Res Rep Urol Year: 2022 Type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Res Rep Urol Year: 2022 Type: Article