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Purple Corn Extract Improves Benign Prostatic Hyperplasia by Regulating Prostate Cell Proliferation and Apoptosis
Hyo-Jung Kim1, Byung-Hak Kim2, Bo-Ram Jin1
1Department of Pharmacology, College of Korean Medicine, Sangji University, 83 Sangjidae-gil, Wonju-si, Gangwon-do 26339, Republic of Korea.
Purple corn extract (PCE) shows promise for treating benign prostatic hyperplasia (BPH). PCE effectively reduces prostate enlargement by modulating key signaling pathways involved in cell proliferation and apoptosis.
Area of Science:
- Pharmacology
- Natural Products
- Urology
Background:
- Purple corn (Zea mays L.) is recognized for its anthocyanin content and traditional medicinal uses.
- Existing research highlights purple corn's benefits for obesity and urinary tract infections, but not for benign prostatic hyperplasia (BPH).
Purpose of the Study:
- To investigate the potential therapeutic effects of purple corn extract (PCE) on benign prostatic hyperplasia (BPH).
- To elucidate the mechanisms by which PCE ameliorates BPH in cellular and animal models.
Main Methods:
- Utilized dihydrotestosterone (DHT)-stimulated WPMY-1 cells and testosterone propionate (TP)-induced rats to model BPH.
- Assessed the impact of PCE on androgen receptor (AR) signaling, phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway, and apoptosis-related gene expression.
- Evaluated changes in prostate weight and histological alterations.
Main Results:
- PCE significantly reduced upregulated androgen receptor (AR) and related gene expression in DHT-stimulated WPMY-1 cells.
- PCE modulated the PI3K/AKT signaling cascade, increasing proapoptotic gene expression.
- PCE administration led to a reduction in prostate weight and restoration of prostate histology in TP-induced rats by inhibiting AR signaling markers.
Conclusions:
- Purple corn extract (PCE) demonstrates a significant ameliorative effect on benign prostatic hyperplasia (BPH).
- PCE alleviates BPH by effectively modulating prostate cell proliferation and apoptosis through the regulation of androgen/AR signaling and the PI3K/AKT pathway.
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