4.7 Article

Therapeutic role of Glycyrrhiza Uralensis fisher on benign prostatic hyperplasia through 5 alpha reductase regulation and apoptosis

期刊

PHYTOMEDICINE
卷 105, 期 -, 页码 -

出版社

ELSEVIER GMBH
DOI: 10.1016/j.phymed.2022.154371

关键词

Benign prostatic hyperplasia; Dihydrotestosterone; Androgen receptor; 5 alpha-reductase 2; Apoptosis; Glycyrrhiza uralensis Fisher

资金

  1. National Research Foundation of Korea [NRF-2018R1A2A3075684, NRF-2021R1A2C1012532, NRF-2021R1A2C2010460]
  2. Korean Ministry of Science, ICT, and Future Planning (MSIP)

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This study found that a water extract of Glycyrrhiza uralensis Fischer has potential therapeutic effects on BPH by inhibiting AR-5AR2 signaling and activating apoptosis signaling to reduce BPH development. Unlike finasteride, GUWE does not impact sperm count, suggesting lower toxicity and a safer alternative option for BPH treatment.
Background: Benign prostatic hyperplasia (BPH) is an age-related disease in adult men. There are two pharmacological treatments for BPH. However, these synthetic materials have various risks, many studies are being conducted to develop new drugs from natural sources. Purpose: In this study, we proposed a beneficial effect of Glycyrrhiza uralensis Fischer on the development and progression of BPH, focusing on the androgen receptor (AR) and 5 alpha-reductase 2 (5AR2) signaling axis. Methods: To explain the therapeutic efficacy of a water extract of G. uralensis (GUWE) for BPH, we used testosterone propionate (TP)-induced BPH rat models and TP-treated RWPE-1 human prostate epithelial cells. Results: In the TP-induced BPH rat models, GUWE reduced the enlarged prostate weight, prostate index, prostate epithelial thickness, and serum DHT levels. In addition, the protein levels of AR and 5AR2 in prostate tissues were significantly decreased by GUWE treatment. Furthermore, GUWE induced apoptosis signaling through an increase of Bcl-2 associated X protein (Bax), caspase 3, and Poly (ADP-ribose) polymerase (PARP) and a decrease of B-cell lymphoma-extra-large (Bcl-xL) in prostate tissues of TP-induced BPH rats. These findings were also confirmed in TP-treated RWPE-1 cells. Fi treatment markedly decreased the sperm count in the epididymis of BPH rats, but GUWE treatment did not affect the sperm count, suggesting less toxicity. Conclusion: These findings suggested that GUWE reduces the development of BPH by inhibiting AR-5AR2 and activating the apoptosis signaling pathway. Furthermore, unlike finasteride, GUWE did not affect sperm count. Therefore, we suggest that GUWE has a potential as a safer alternative option for BPH treatment.

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