神经毒性
PI3K/AKT/mTOR通路
蛋白激酶B
化学
癌症研究
毒素
神经科学
药理学
细胞生物学
医学
生物
信号转导
生物化学
毒性
有机化学
作者
Xiukuan Li,Jinyun Long,Chunyan Yao,Xiaoling Liu,Na Li,Yukui Zhang,Tongjian Cai,Guiyuan Xiong,K. Wang,Yuhui Hao,Ka Chen,Zuping Zhou,Tongjian Cai,Peng Luo,Tongjian Cai
标识
DOI:10.1016/j.toxlet.2024.08.003
摘要
T-2 toxin is one of the mycotoxins widely distributed in human food and animal feed. Our recent work has shown that microglial activation may contribute to T-2 toxin-induced neurotoxicity. However, the molecular mechanisms involved need to be further clarified. To address this, we employed high-throughput transcriptome sequencing and found altered B cell translocation gene 2 (BTG2) expression levels in microglia following T-2 toxin treatment. It has been shown that altered BTG2 expression is involved in a range of neurological pathologies, but whether it's involved in the regulation of microglial activation is unclear. The aim of this study was to investigate the role of BTG2 in T-2 toxin-induced microglial activation. The results of animal experiments showed that T-2 toxin caused neurobehavioral disorders and promoted the expression of microglial BTG2 and pro-inflammatory activation of microglia in hippocampus and cortical, while microglial inhibitor minocycline inhibited these changes. The results of in vitro experiments showed that T-2 toxin enhanced BTG2 expression and pro-inflammatory microglial activation, and inhibited BTG2 expression weakened T-2 toxin-induced microglial activation. Moreover, T-2 toxin activated PI3K/AKT and its downstream NF-κB signaling pathway, which could be reversed after knock-down of BTG2 expression. Meanwhile, the PI3K inhibitor LY294002 also blocked this process. Therefore, BTG2 may be involved in T-2 toxin's ability to cause microglial activation through PI3K/AKT/NF-κB pathway.
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