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异氟烷预处理通过 TLR4/NFB 信号通路减轻电磁脉冲诱导的脑损伤。

Isoflurane Preconditioning Attenuates Brain Injury Induced by Electromagnetic Pulse via the TLR4/NFB Signaling Pathway.

机构信息

Department of Anesthesiology, The Second Affiliated Hospital of Air Force Medical University, Xi'an 710038, China.

Department of Anesthesiology, Xiang'an Hospital of Xiamen University, Xiamen 361101, China.

出版信息

Oxid Med Cell Longev. 2019 Jan 6;2019:9653494. doi: 10.1155/2019/9653494. eCollection 2019.

DOI:10.1155/2019/9653494
PMID:30723536
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6339739/
Abstract

Electromagnetic pulse (EMP) is a unique type of electromagnetic radiation, and EMP exposure causes a series of biological effects. The nervous system is sensitive to EMP. We studied the neuroprotective effects of isoflurane preconditioning against EMP exposure and used hematoxylin-eosin staining (HE) to observe the effects of electromagnetic pulse and isoflurane preconditioning on neurons. Inflammatory cytokines were detected by enzyme-linked immunosorbent assay (ELISA). Western blotting was used to detect the expression of caspase-3, CD11b, TLR4, and NFBp65. We found that after EMP exposure, the number of abnormal neurons had increased, and the expression of caspase-3, CD11b, TLR4, and NFBp65 had also increased. Isoflurane preconditioning can reverse the above phenomenon. Moreover, we found that isoflurane preconditioning can reduce neuronal apoptosis and improve cognitive impairment induced by EMP. These findings indicate that isoflurane preconditioning can protect neurons in the cerebral cortex from EMP exposure, alleviate the inflammatory reaction and cell apoptosis, and improve cognitive impairment induced by EMP. These effects may occur through the downregulation of the TLR4/NFB signaling pathway and the inhibition of microglial activation.

摘要

电磁脉冲(EMP)是一种独特类型的电磁辐射,EMP 暴露会引起一系列生物效应。神经系统对 EMP 敏感。我们研究了异氟醚预处理对 EMP 暴露的神经保护作用,并使用苏木精-伊红染色(HE)观察电磁脉冲和异氟醚预处理对神经元的影响。通过酶联免疫吸附试验(ELISA)检测炎性细胞因子。通过 Western blot 检测 caspase-3、CD11b、TLR4 和 NFBp65 的表达。我们发现,EMP 暴露后,异常神经元数量增加,caspase-3、CD11b、TLR4 和 NFBp65 的表达也增加。异氟醚预处理可以逆转上述现象。此外,我们发现异氟醚预处理可以减少神经元凋亡并改善 EMP 引起的认知障碍。这些发现表明,异氟醚预处理可以保护大脑皮质神经元免受 EMP 暴露,减轻炎症反应和细胞凋亡,并改善 EMP 引起的认知障碍。这些作用可能通过 TLR4/NFB 信号通路的下调和小胶质细胞激活的抑制来实现。

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