Chrysin attenuates testosterone-induced benign prostate hyperplasia in rats

Food Chem Toxicol. 2018 Jan:111:650-659. doi: 10.1016/j.fct.2017.12.017. Epub 2017 Dec 14.

Abstract

Benign prostate hyperplasia (BPH) is a common age-related health problem affecting almost 3 out of 4 men in their sixties. Chrysin is a dietary phytoestrogen found naturally in bee propolis and various plant extracts. It possesses antioxidant, anti-inflammatory and anti-proliferative properties. The current study was conducted to explore the role chrysin plays in protection against testosterone-induced BPH in rats. On grounds of a preliminary experiment, a dose of chrysin (50 mg/kg) was chosen for further investigation. Testosterone significantly depleted glutathione, suppressed superoxide dismutase and catalase activities, and elevated lipid peroxidation. Moreover, it markedly scaled down the level of cleaved caspase-3 enzyme, reduced Bax/Bcl-2 ratio and mRNA expression of p53 and p21; conversely, protein expression of proliferating cell nuclear antigen was enhanced. Chrysin alleviated testosterone-induced oxidative stress and restored cleaved caspase-3 level, Bax/Bcl-2 ratio and mRNA expression of p53 and p21 to almost control levels. Chrysin prevented the increase in binding activity of nuclear factor kappa B (NF-κB) p65 subunit, mRNA expression of insulin-like growth factor 1 (IGF-1) and insulin-like growth factor 1 receptor (IGF-1R). These data highlight the protective role of chrysin against experimentally-induced BPH. This is attributed - at least partly - to its antioxidant, antiproliferative and proapoptotic properties.

Keywords: BPH; Chrysin; Prostate; Rats; Testosterone.

MeSH terms

  • Animals
  • Caspase 3 / genetics
  • Caspase 3 / metabolism
  • Flavonoids / administration & dosage*
  • Glutathione / metabolism
  • Humans
  • Insulin-Like Growth Factor I / metabolism
  • Male
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Proliferating Cell Nuclear Antigen / genetics
  • Proliferating Cell Nuclear Antigen / metabolism
  • Prostatic Hyperplasia / chemically induced
  • Prostatic Hyperplasia / drug therapy*
  • Prostatic Hyperplasia / genetics
  • Prostatic Hyperplasia / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Somatomedin / genetics
  • Receptors, Somatomedin / metabolism
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / metabolism
  • Testosterone / adverse effects*

Substances

  • Flavonoids
  • NF-kappa B
  • Proliferating Cell Nuclear Antigen
  • Receptors, Somatomedin
  • chrysin
  • Testosterone
  • Insulin-Like Growth Factor I
  • Superoxide Dismutase
  • Caspase 3
  • Glutathione