Heat-Killed and Live Enterococcus faecalis Attenuates Enlarged Prostate in an Animal Model of Benign Prostatic Hyperplasia

J Microbiol Biotechnol. 2021 Aug 28;31(8):1134-1143. doi: 10.4014/jmb.2102.02032.

Abstract

In the present study, we investigated the inhibitory effect of heat-killed Enterococcus faecalis (E. faecalis) and live E. faecalis on benign prostatic hyperplasia (BPH). The BPH rat model was established by administering male rats with testosterone propionate (TP, 5 mg/kg, in corn oil) via subcutaneous injections daily for four weeks after castration. The rats were divided into five groups: Con, corn oil-injected (s.c.) + DW administration; BPH, TP (5 mg/kg, s.c.) + DW administration; BPH+K_EF, TP (5 mg/kg, s.c.) + heat-killed E. faecalis (7.5 × 1012 CFU/g, 2.21 mg/kg) administration; BPH+L_EF, TP (5 mg/kg, s.c.) + live E. faecalis (1 × 1011 CFU/g, 166 mg/kg) administration; BPH+Fi, TP (5 mg/kg, s.c.) + finasteride (1 mg/kg) administration. In both of BPH+K_EF and BPH+L_EF groups, the prostate weight decreased and histological changes due to TP treatment recovered to the level of the Con group. Both of these groups also showed regulation of androgen-signaling factors, growth factors, and apoptosis-related factors in prostate tissue. E. faecalis exhibited an inhibitory effect on benign prostatic hyperplasia, and even heat-killed E. faecalis showed similar efficacy on the live cells in the BPH rat model. As the first investigation into the effect of heat-killed and live E. faecalis on BPH, our study suggests that heat-killed E. faecalis might be a food additive candidate for use in various foods, regardless of heat processing.

Keywords: Benign prostatic hyperplasia; Enterococcus faecalis; heat-killed microorganism.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Dihydrotestosterone / metabolism
  • Disease Models, Animal
  • Enterococcus faecalis*
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Hot Temperature
  • Male
  • Phosphorylation
  • Probiotics / therapeutic use*
  • Prostate / drug effects
  • Prostate / metabolism
  • Prostate / pathology
  • Prostatic Hyperplasia / chemically induced
  • Prostatic Hyperplasia / metabolism
  • Prostatic Hyperplasia / pathology*
  • Prostatic Hyperplasia / therapy*
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Androgen / metabolism
  • Signal Transduction / drug effects
  • Signal Transduction / genetics
  • Testosterone Propionate / pharmacology

Substances

  • Receptors, Androgen
  • Dihydrotestosterone
  • Extracellular Signal-Regulated MAP Kinases
  • Testosterone Propionate