Baicalin alleviates benign prostate hyperplasia through androgen-dependent apoptosis

Area of Science:

• Pharmacology
• Cell Biology
• Urology

Background:

• Benign prostatic hyperplasia (BPH) is a common condition in aging men, characterized by prostate tissue overgrowth.
• The exact molecular causes of BPH are not fully understood, limiting effective treatment options.
• Baicalin has shown therapeutic potential in various diseases, but its effects on BPH were unexplored.

Purpose of the Study:

• To investigate the therapeutic potential of baicalin in benign prostatic hyperplasia (BPH).
• To elucidate the mechanism of action of baicalin in BPH development.
• To evaluate baicalin's effects in both animal models and cell line studies.

Main Methods:

• Established a testosterone-induced rat model for BPH and used DHT-stimulated RWPE-1 and WPMY-1 prostate cell lines.
• Administered baicalin to the animal model and treated the cell lines.
• Analyzed prostate size, DHT levels, 5α-reductase Type II activity, apoptosis markers (Bax/Bcl-2 ratio, caspase-3, caspase-8), AMPK phosphorylation, and expression of AR, PSA, PCNA, and Bcl-2.

Main Results:

• Baicalin administration reduced prostate enlargement, suppressed DHT production, and inhibited 5α-reductase Type II activity in vivo.
• Baicalin demonstrated anti-proliferative effects by modulating the Bax/Bcl-2 ratio, activating caspases, and inducing AMPK phosphorylation.
• In vitro, baicalin reduced the overexpression of androgen receptor (AR), prostate-specific antigen (PSA), proliferating cell nuclear antigen (PCNA), and Bcl-2 in DHT-stimulated prostate cells.

Conclusions:

• Baicalin exhibits therapeutic effects against benign prostatic hyperplasia (BPH).
• Baicalin suppresses androgen-dependent BPH development through apoptosis induction.
• Baicalin presents a promising therapeutic agent for BPH, acting both in vivo and in vitro.