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

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-KB phosphorylation in BV2 microglia cells. However, the addition of active oxygen scavenger Nacetylcysteine can significantly reduce the ROS production, improve cell cycle arrest, reduce apoptosis, and the expression of phosphorylated NF-KB in BV2 microglia cells. These results indicate that AFB1 induces microglia cells apoptosis through oxidative stress by activating NF-KB signaling pathway.

Automated summary

Studies have shown that aflatoxin B1 (AFB1) can induce cytotoxicity in various cells and organs through oxidative stress. However, the toxic effects and mechanism of AFB1 on microglia cells in the spinal cords have not been studied yet. This study found that AFB1 significantly reduced the number of microglia cells and altered the levels of oxidants and antioxidants in the spinal cords of mice. Furthermore, AFB1 induced oxidative stress, promoted apoptosis and cell cycle arrest, and activated NF-KB phosphorylation in BV2 microglia cells. The addition of an active oxygen scavenger effectively reduced these effects. These findings suggest that AFB1 induces microglia cell apoptosis through oxidative stress via the NF-KB signaling pathway.