Department of Histology and Embryology, Binzhou Medical University, China.
Key Laboratory for Robot & Intelligent Technology of Shandong Province, Shandong University of Science and Technology, China.
Environ Toxicol Pharmacol. 2022 Feb;90:103794. doi: 10.1016/j.etap.2021.103794. Epub 2021 Dec 29.
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.
许多研究表明，黄曲霉毒素 B1（AFB1）可通过氧化应激引起许多细胞和器官的细胞毒性。然而，AFB1 对脊髓中的小胶质细胞的毒性作用及相关机制尚未得到研究。我们的结果表明，AFB1 显著降低了小鼠脊髓中小胶质细胞的数量，增加了氧化剂（丙二醛和过氧化氢），但降低了抗氧化剂（超氧化物歧化酶和总抗氧化能力），呈剂量依赖性。此外，AFB1 显著增加了氧化应激，促进了 BV2 小胶质细胞的细胞凋亡和 G2-M 期细胞周期阻滞，并激活了 NF-κB 的磷酸化。然而，添加活性氧清除剂 N-乙酰半胱氨酸可以显著减少 ROS 的产生，改善细胞周期阻滞，减少细胞凋亡，降低 BV2 小胶质细胞中磷酸化 NF-κB 的表达。这些结果表明，AFB1 通过激活 NF-κB 信号通路诱导小胶质细胞凋亡。
