Neuroprotective Effects of Heat-Killed Levilactobacillus brevis KU15152 on H2O2-Induced Oxidative Stress

J Microbiol Biotechnol. 2023 Sep 28;33(9):1189-1196. doi: 10.4014/jmb.2304.04045. Epub 2023 May 29.

Abstract

This study proposed to demonstrate the neuroprotective effects of heat-killed Levilactobacillus brevis KU15152. Heat-killed L. brevis KU15152 showed antioxidant activity similar to that of Lacticaseibacillus rhamnosus GG, in terms of radical scavenging activity. To evaluate the neuroprotective effects, conditioned medium (CM) obtained by incubating heat-killed bacteria in intestinal cells (HT-29) was used through gut-brain axis. CM from L. brevis KU15152 protected neuroblastoma cells (SH-SY5Y) against H2O2-induced oxidative stress. Pretreatment with CM significantly alleviated the morphological changes induced by H2O2. Heat-killed L. brevis KU15152 showed an increased brain-derived neurotrophic factor (BDNF) expression in HT-29 cells. L. brevis KU15152-CM remarkably downregulated the Bax/Bcl-2 ratio, while upregulating the expression of BDNF and tyrosine hydroxylase (TH) in SH-SY5Y cells. Furthermore, L. brevis KU15152-CM reduced caspase-3 activity following H2O2 treatment. In conclusion, L. brevis KU15152 can be potentially used as food materials to avoid neurodegenerative diseases.

Keywords: Levilactobacillus brevis; gut–brain axis; heat-killed probiotics; neuroprotective effect; oxidative stress.

MeSH terms

  • Brain-Derived Neurotrophic Factor
  • Hot Temperature
  • Humans
  • Hydrogen Peroxide / pharmacology
  • Levilactobacillus brevis*
  • Neuroblastoma*
  • Neuroprotective Agents* / pharmacology
  • Oxidative Stress

Substances

  • Hydrogen Peroxide
  • Neuroprotective Agents
  • Brain-Derived Neurotrophic Factor