Related Experiment Video
Updated: Oct 8, 2025
Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
Published on: November 6, 2017
Aflatoxin B1 induces microglia cells apoptosis mediated by oxidative stress through NF-κB signaling pathway in mice
Yanqiu Zhou1, Siyuan Wang1, Hanlin Luo1
1Department of Histology and Embryology, Binzhou Medical University, China.
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.
Insights
Aflatoxin B1 (AFB1) harms spinal cord microglia by increasing oxidative stress and apoptosis. N-acetylcysteine protects these cells, indicating AFB1
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Aflatoxin B1 (AFB1) is a known cytotoxic agent inducing oxidative stress.
- The effects of AFB1 on spinal cord microglia remain uninvestigated.
Purpose of the Study:
- To elucidate the toxic effects and underlying mechanisms of AFB1 on microglia in the spinal cord.
- To investigate AFB1-induced oxidative stress, apoptosis, and cell cycle arrest in BV2 microglia cells.
Main Methods:
- Dose-dependent administration of AFB1 to mice spinal cords and BV2 microglia cells.
- Measurement of oxidant and antioxidant levels.
- Assessment of apoptosis, cell cycle, and NF-κB signaling pathway activation.
- Evaluation of N-acetylcysteine's protective effects.
Main Results:
- AFB1 reduced microglia cell numbers and altered oxidant/antioxidant balance in mice spinal cords.
- AFB1 induced oxidative stress, apoptosis, G2-M cell cycle arrest, and NF-κB activation in BV2 cells.
- N-acetylcysteine mitigated AFB1-induced ROS production, apoptosis, and NF-κB phosphorylation.
Conclusions:
- AFB1 induces microglia apoptosis in the spinal cord via oxidative stress.
- Activation of the NF-κB signaling pathway is a key mechanism in AFB1-induced microglia apoptosis.
More Related Videos
Related Concept Videos
02:26NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
01:31The Intrinsic Apoptotic Pathway