Korean researchers report that a naturally occurring compound, chrysophanic acid, reduced prostate weight in a rat model of benign prostatic hyperplasia (BPH), suggesting that the compound might classify as a potential new treatment.
The study, “Chrysophanic acid reduces testosterone-induced benign prostatic hyperplasia in rats by suppressing 5α-reductase and extracellular signal-regulated kinase,” was published in the journal Oncotarget.
Since current drug treatments with alpha-blockers and 5-alpha reductase inhibitors are linked to an array of side effects, researchers are on the lookout for new ways of treating lower urinary tract symptoms caused by BPH. Many natural compounds under investigation are reported to show beneficial effects on prostate size or BPH symptoms.
Researchers at Kyung Hee University in Korea explored chrysophanic acid’s potential in treating BPH. (The compound is a member of the anthraquinone family, and previous studies have shown anthraquinone derivatives demonstrate anti-cancer, antimicrobial and anti-inflammatory effects.) The researchers triggered BPH in the rats by injecting testosterone over four weeks.
The team compared chrysophanic acid treatment outcomes to that of finasteride, an approved BPH treatment sold under the brand name Proscar (and as Propecia to treat male pattern baldness), and to those seen in untreated control animals.
Treatment with chrysophanic acid lowered the prostate weight by a similar amount as finasteride, and also reversed cellular changes in the prostate. While BPH rats had thicker layers of prostate epithelial cells and a smaller prostate lumen, both chrysophanic acid and finasteride reversed the changes.
The rat version of prostate-specific antigen (PSA) also lowered using both treatments. In addition, the treatments reduced the levels of 5-alpha reductase — the enzyme producing the BPH-driving type of testosterone known as dihydrotestosterone.
Researchers then performed a molecular analysis of factors known to be involved in BPH. Both treatments lowered the increase in ER-alpha, androgen receptor numbers, and the androgen receptor-associated factor SRC1 that was seen in the testosterone-treated rats. Similarly, molecular signaling cascades were normalized.
To aid future research, the team also established a cell model of BPH by treating human prostate epithelial cells with high levels of testosterone. Studies showed that chrysophanic acid lowered the cells’ multiplication rate. The team also observed that chrysophanic acid induced in the cells several changes previously noted in the rats, including lower PSA production.
“Overall,” the researchers concluded, “these results suggest a potential pharmaceutical feature of CA [chrysophanic acid] in the treatment of BPH.”