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<p>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&#xa0;mg/kg body weight/day), BPH + myricetin group, which received myricetin (50&#xa0;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&#xa0;mg/kg. After 28&#xa0;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 <i>5-α reductase</i> enzyme, and the androgen receptor (<i>AR</i>), while simultaneously increasing the prostatic mRNA expression levels of the pro-apoptotic protein <i>Bax</i>. 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 (<i>VEGF-A</i>) mRNA expression levels. In summary, myricetin displays potential as a BPH therapy by diminishing inflammation and oxidative stress, hindering <i>5-α reductase</i>/<i>AR</i>/DHT signaling, and endorsing pro-apoptotic over anti-apoptotic pathways.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月7日

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  • Ghada Alomari,
  • Bahaa Al-Trad,
  • Janti Qar,
  • Lena Tahat,
  • Yazan Abu Haija,
  • Aseel Al-najjar,
  • Ibrahim Albokhadaim,
  • Saad Shousha,
  • Ahmed O. Alameen,
  • Mustafa Shukry

摘要

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-α reductase 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-α reductase/AR/DHT signaling, and endorsing pro-apoptotic over anti-apoptotic pathways.