Journal
NUTRIENTS
Volume 13, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/nu13030884
Keywords
Phyllostachys pubescens; benign prostatic hyperplasia; 5α -reductase type 2; dihydrotestosterone
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Funding
- Korea Institute of Oriental Medicine [KSN20134262]
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The study found that bamboo leaves extract (PPE) inhibited the activity and mRNA expression of human SRD5A2, providing a protective effect in a testosterone-induced BPH rat model. PPE treatment reduced prostate weight, serum hormone levels, and expression of specific genes related to prostate growth and inflammation, indicating its potential as a therapeutic agent for BPH.
Benign prostatic hyperplasia (BPH) is the most common symptomatic abnormality of the human prostate characterized by uncontrolled proliferation of the prostate gland. In this study, we investigated the effect of bamboo, Phyllostachys pubescens, leaves extract (PPE) on human 5 alpha-reductase type 2 (SRD5A2) gene promoter activity in human prostate cell lines and the protective effect of PPE on a testosterone-induced BPH rat model. PPE repressed human SRD5A2 promoter activity and its mRNA expression. The rats treated with PPE for 4 weeks showed a significantly attenuated prostate weight compared to vehicle control. PPE-treated rats also showed reduced serum dihydrotestosterone, testosterone, prostate-specific antigen, and SRD5A2 levels by testosterone injection. Quantitative real-time polymerase chain reaction showed that PPE treatment significantly decreased mRNA expression of SRD5A2, androgen receptor (AR), proliferating cell nuclear antigen (PCNA), and fibroblast growth factor 2 compared with the vehicle-treated, testosterone-injected rats in the prostate. Furthermore, PPE treatment showed reduced AR, PCNA, and tumor necrosis factor alpha expression in the prostate via immunohistofluorescence staining. In conclusion, oral administration of PPE prevented and inhibited the development and progression of enlarged prostate lesions in testosterone-induced animal models through various anti-proliferative and anti-inflammatory pharmacological effects and induced suppression of SRD5A2 gene expression.
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