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BACKGROUND/OBJECTIVES: (EAR), which is traditionally used to treat various diseases, on BPH development using a testosterone-induced BPH model. MATERIALS/METHODS: . 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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Hwangbo et al. (2024) studied this question.
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