Nutr Res Pract.
2024 Dec;18(6):793-805. 10.4162/nrp.2024.18.6.793.
Asparagi radix alleviates testosterone-induced benign prostatic hyperplasia by inhibiting 5α-reductase activity and androgen receptor signaling pathway
- Affiliations
-
- 1Department of Biochemistry, Dong-eui University College of Korean Medicine, Busan 47227, Korea
- 2Basic Research Laboratory for the Regulation of Microplastic-Mediated Diseases and Anti-Aging Research Center, Dong-eui University, Busan 47227, Korea
- 3Department of Parasitology and Genetics, Kosin University College of Medicine, Busan 49104, Korea
- 4Department of Food Science & Nutrition, Tongmyong University, Busan 48520, Korea
- 5Hamsoapharm Central Research, Jinan 55442, Korea
- 6Department of Biological Sciences, College of Natural Sciences, Pusan National University, Busan 46241, Korea
- 7Department of Food and Nutrition, Chung-Ang University, Ansung 17546, Korea
- 8Department of Marine Life Science, Jeju National University, Jeju 63243, Korea
- KMID: 2562367
- DOI: http://doi.org/10.4162/nrp.2024.18.6.793
Abstract
- BACKGROUND/OBJECTIVES
Recently, herbal medicines have gained attention for the treatment of benign prostatic hyperplasia (BPH), a common disease in elderly men. In this study, we aimed to determine the effect of ethanol extract of Asparagi radix (EAR), which is traditionally used to treat various diseases, on BPH development using a testosteroneinduced BPH model.
MATERIALS/METHODS
Testosterone propionate (TP)-treated Sprague–Dawley rats were used to establish a BPH model in vivo. EAR was orally administered along with TP, and finasteride was used as a positive control. All rats were sacrificed at the end of the experiment, and pathological changes in the prostate tissue and levels of key biomarkers associated with BPH pathogenesis were assessed.
RESULTS
Oral administration of EAR significantly inhibited TP-induced BPH by reducing the prostate weight, lumen size, and epithelial thickness in a concentration-dependent manner. EAR also significantly abrogated the expression of 5α-reductase type 2 (SRD5A2), proliferating cell nuclear antigen, and prostate-specific antigen (PSA) induced by TP. Additionally, serum levels of testosterone, dihydrotestosterone, and PSA were elevated in the TP-induced group but decreased in the EAR-treated group. EAR also decreased the expression levels of the androgen receptor (AR) and its coactivators in TP-induced BPH model rats.
CONCLUSION
Our findings revealed that EAR protected against BPH by inhibiting 5α-reductase activity and AR signaling pathway, suggesting its potential for BPH treatment.
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