Aflatoxin B1 induces microglia cells apoptosis mediated by oxidative stress through NF-κB signaling pathway in mice spinal cords

Environ Toxicol Pharmacol. 2022 Feb:90:103794. doi: 10.1016/j.etap.2021.103794. Epub 2021 Dec 29.

Abstract

Many studies have shown that aflatoxin B1 (AFB1) can cause cytotoxicity in numerous cells and organs induced by oxidative stress. However, the toxic effects and related mechanism of AFB1 on the microglia cells in the spinal cords have not been studied yet. Our results showed that AFB1 significantly reduced the number of microglia cells, increased the oxidants (malonaldehyde and hydrogen peroxide) but decreased the anti-oxidants (superoxide dismutase and total antioxidant capacity) in a dose dependent manner in mice spinal cords. In addition, AFB1 significantly increased the oxidative stress, promoted apoptosis and cell cycle arrest in G2-M phase, and activated NF-κB phosphorylation in BV2 microglia cells. However, the addition of active oxygen scavenger N-acetylcysteine can significantly reduce the ROS production, improve cell cycle arrest, reduce apoptosis, and the expression of phosphorylated NF-κB in BV2 microglia cells. These results indicate that AFB1 induces microglia cells apoptosis through oxidative stress by activating NF-κB signaling pathway.

Keywords: Aflatoxin B1; Apoptosis; Microglia cells; NF-κB; Oxidative stress.

MeSH terms

  • Acetylcysteine / administration & dosage
  • Aflatoxin B1 / toxicity*
  • Animals
  • Apoptosis / drug effects*
  • Cell Cycle Checkpoints / drug effects
  • Cells, Cultured
  • Male
  • Mice
  • Microglia / drug effects*
  • NF-kappa B / metabolism
  • Oxidative Stress / drug effects
  • Phosphorylation
  • Reactive Oxygen Species / metabolism
  • Signal Transduction
  • Spinal Cord / drug effects

Substances

  • NF-kappa B
  • Reactive Oxygen Species
  • Aflatoxin B1
  • Acetylcysteine