Myricetin alleviates testosterone-induced benign prostatic hyperplasia.

Myricetin alleviates testosterone-induced benign prostatic hyperplasia by attenuating inflammation, oxidative stress, apoptosis and androgen signaling.

Ghada Alomari, B Al-Trad, Janti Qar, Lena Tahat, Yazan Abu Haija, Aya H Al-Najjar, Ibrahim Albokhadaim, Saad Shousha, Ahmed O Alameen, Mustafa Shukry

Sci Rep

Apr 6, 2026

Sources

0:00 / 0:00

Sign in to access this feature

Create a free account or sign in to use AI summaries, listen to articles, download PDFs, and save to your library.

182 views

Abstract

This study investigates the effect of myricetin as a therapeutic for benign prostatic hyperplasia (BPH) disease using a testosterone-induced BPH animal model. Forty adult male rats were randomly divided into four groups as follows: control group, BPH group that was injected with testosterone subcutaneously (3 mg/kg body weight/day), BPH + myricetin group, which received myricetin (50 mg/kg) subcutaneously every day with the BPH induction, and BPH + finasteride group, which administered finasteride orally with the BPH induction at a daily dose of 5 mg/kg. After 28 days, blood and prostate tissue samples were collected for analysis. Compared to the control group, treatment with myricetin improved the pathohistological signs of BPH and enhanced the antioxidant and anti-inflammatory capacity of the prostatic tissue, as evidenced by its ability to enhance the total antioxidant capacity (TAC) levels and reduce malondialdehyde (MDA) levels, decrease the levels of the inflammatory biomarkers tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL1-β) levels, and reduce serum dihydrotestosterone (DHT) levels. In addition, myricetin treatment showed beneficial effects through its ability to reduce the prostatic mRNA expression levels of the anti-apoptotic protein Bcl2, the 5-αreductase enzyme, and the androgen receptor (AR), while simultaneously increasing the prostatic mRNA expression levels of the pro-apoptotic protein Bax. Myricetin treatment also exhibited anti-proliferative and anti-angiogenic effects, as evidenced by the reduced prostatic proliferating cell nuclear antigen (PCNA) and vascular endothelial growth factor-A (VEGF-A) mRNA expression levels. In summary, myricetin displays potential as a BPH therapy by diminishing inflammation and oxidative stress, hindering 5-αreductase/AR/DHT signaling, and endorsing pro-apoptotic over anti-apoptotic pathways.