Abstract
Benign prostatic hyperplasia (BPH) is a common chronic disease of the urinary system among elderly men. Especially, the metabolic imbalance of androgen in elderly men is one of the leading causes of BPH. Dihydrotestosterone (DHT) and converted testosterone by 5-α reductase type 2 (5AR2), binding with androgen receptor (AR), affect prostate proliferation and growth. In BPH, levels of androgen signaling-related protein expression are shown highly. Androgen signaling induces the overexpression of prostate-specific antigen (PSA) and cell proliferation factor such as proliferating cell nuclear antigen (PCNA) and cyclin D1. Grape skin anthocyanins are well known for their antioxidative, anti-cancer, anti-diabetes, anti-inflammatory, antimicrobial, and anti-aging activities. Polymerized anthocyanin (PA) downregulated the expression of androgen signaling-related proteins such as 5AR2, AR, and PSA in LNCaP cell lines. Furthermore, we investigated the effects on PA in testosterone propionate-induced BPH rat experiments. The oral administration of PA decreased the prostate weight in rats with TP-induced BPH. PA decreased the AR, 5AR2, SRC1, PSA, PCNA, and cyclin D1 expression in prostate tissues and the serum DHT levels, ameliorated the BPH-mediated increase of Bcl-2 expression, and increased the Bax expression. These results suggest that PA may be a potential natural therapeutic agent for BPH treatment.
Highlights
Benign prostatic hyperplasia (BPH) is a common chronic disease of the urinary system among men aged over 50 years [1]; it is characterized by the increased proliferation of smooth muscle cells, stromal cells, and epithelial cells in the prostate gland
During BPH, androgens promote the proliferation of epithelial cells or stromal cells in the prostate gland in an autocrine or paracrine manner, leading to the imbalance in prostate cell proliferation and apoptosis; this has been considered an important cause of BPH [6]
testosterone propionate (TP) treatment significantly upregulated the expression of androgen receptor (AR), 5AR2, and prostate-specific antigen (PSA) in the LNCaP cells
Summary
Benign prostatic hyperplasia (BPH) is a common chronic disease of the urinary system among men aged over 50 years [1]; it is characterized by the increased proliferation of smooth muscle cells, stromal cells, and epithelial cells in the prostate gland. The fundamental cause of BPH is unknown, it has been well established that the prostate gland in aging men is affected by androgens [5]. During BPH, androgens promote the proliferation of epithelial cells or stromal cells in the prostate gland in an autocrine or paracrine manner, leading to the imbalance in prostate cell proliferation and apoptosis; this has been considered an important cause of BPH [6]. Dihydrotestosterone (DHT) and testosterone (TST) are well known to be associated with the development of BPH [7]. DHT is a more potent androgen compared to TST because of its higher binding for the androgen receptor (AR) [8]. 5-α reductase type 2 (5AR2) converts
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