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烯胺暴露通过PI3K/Akt/NF-κB途径诱导神经毒性:来自网络毒理学和实验验证的证据

Zhaoda Duan¹, Chunjiao Yu¹, Qiuxian Yu²

¹Institute of Biomedical Engineering, Kunming Medical University, Kunming 650500, PR China.

Ecotoxicology and environmental safety

|February 24, 2026

概括

烯胺 (ACR) 暴露会通过破坏海马神经元并激活生存和炎症通路而引起神经毒性. 这项研究揭示了ACRR.

科学领域:

神经科学是一个神经科学.
毒理学毒理学毒理学
分子生物学分子生物学

背景情况:

烯胺 (ACR) 是一个无处不在的工业和食品加工化学物质.
在ACR诱导的神经毒性的基础上,确切的机制仍然不完全理解.
调查ACR的神经毒性作用对于公共健康和安全至关重要.

研究的目的:

阐明烯胺诱导的神经毒性的分子机制.
确定关键的分子标和参与ACR神经毒性的途径.
为潜在的预防策略提供理论基础,防止ACR神经毒性.

主要方法:

网络毒理学和数据库分析以确定与ACR相关的和神经毒性目标.
分子对接和动力学模拟以预测ACR蛋白相互作用.
在体内和体外实验验证使用细胞活力测定,细胞亡和信号通路分析.

主要成果:

确定了100个重叠的基因,这些基因富含PI3K/Akt信号和亡途径.
在活体中,ACR暴露导致海马神经元损伤.
在体外,ACR暴露降低了细胞活力,增加了细胞亡和炎症,激活PI3K/Akt和NF-κB通路.

结论:

由ACR诱导的神经毒性涉及生存和炎症-亡信号通路之间的复杂相互作用.
PI3K/Akt和NF-κB信号通路是ACR神经毒性的关键调解者.
了解这些机制为治疗ACR暴露的治疗干预提供了潜在的途径.

关键词:

烯胺是什么烯胺是什么细胞灭亡 (apoptosis) 是一种死亡的过程.网络毒理学网络毒理学神经炎症是一种神经炎症.在PI3K/Akt/NF-κB路径中.

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