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小胶质细胞介导的神经炎症负调控在改善癫痫发作后情绪行为中的作用

The Role of the Negative Regulation of Microglia-Mediated Neuroinflammation in Improving Emotional Behavior After Epileptic Seizures.

作者信息

Wu Qiong, Wang Hua, Liu Xueyan, Zhao Yajuan, Zhang Junmei

机构信息

Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China.

出版信息

Front Neurol. 2022 Apr 14;13:823908. doi: 10.3389/fneur.2022.823908. eCollection 2022.

DOI:10.3389/fneur.2022.823908
PMID:35493845
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9046666/
Abstract

OBJECTIVE

Studies have long shown that uncontrolled inflammatory responses in the brain play a key role in epilepsy pathogenesis. Microglias play an important role in epileptic-induced neuroinflammation, but their role after epileptic seizures is still poorly understood. Alleviating epilepsy and its comorbidities has become a key area of interest for pediatricians.

METHODS

A pilocarpine-induced rat model of epilepsy was established. The rats were randomly divided into four groups: a control group, epilepsy group, TLR4 inhibitor group (epilepsy+TAK-242), and NF-κB antagonist group (epilepsy+BAY11-7082).

RESULTS

  1. The results of TUNEL staining showed that the expression in rats in the epilepsy group was the most obvious and was significantly different from that in rats in the control, EP+BAY and EP+TAK groups. 2. The expression of TLR4 and NF-κB was highest in rats in the epilepsy group and was significantly different from that in rats in the control, EP+BAY and EP+TAK groups. 3. The fluorescence intensity and number of IBA-1-positive cells in rats in the epilepsy group were highest and significantly different from those in rats in the control, EP+BAY and EP+TAK groups. Western blot analysis of IBA-1 showed that the expression in rats in the epilepsy group was the highest and was statistically significant. 4. CD68 was the highest in rats in the epilepsy group and was statistically significant. 5. In the open-field experiment, the central region residence time of rats in the EP group was delayed, the central region movement distance traveled was prolonged, the total distance traveled was prolonged, and the average speed was increased. Compared with rats in the EP group, rats in the EP+BAY and EP+ TAK groups exhibited improvements to different degrees.

CONCLUSION

At the tissue level, downregulation of the TLR4/NF-κB inflammatory pathway in epilepsy could inhibit microglial activation and the expression of the inflammatory factor CD68, could inhibit hyperphagocytosis, and inhibit the occurrence and exacerbation of epilepsy, thus improving cognitive and emotional disorders after epileptic seizures.

摘要

目的

长期以来的研究表明，大脑中不受控制的炎症反应在癫痫发病机制中起关键作用。小胶质细胞在癫痫诱导的神经炎症中起重要作用，但其在癫痫发作后的作用仍知之甚少。减轻癫痫及其合并症已成为儿科医生关注的关键领域。

方法

建立毛果芸香碱诱导的大鼠癫痫模型。将大鼠随机分为四组：对照组、癫痫组、TLR4抑制剂组（癫痫+TAK-242）和NF-κB拮抗剂组（癫痫+BAY11-7082）。

结果

  1. TUNEL染色结果显示，癫痫组大鼠的表达最明显，与对照组、EP+BAY组和EP+TAK组大鼠有显著差异。2. TLR4和NF-κB在癫痫组大鼠中的表达最高，与对照组、EP+BAY组和EP+TAK组大鼠有显著差异。3. 癫痫组大鼠中IBA-1阳性细胞的荧光强度和数量最高，与对照组、EP+BAY组和EP+TAK组大鼠有显著差异。IBA-1的蛋白质免疫印迹分析显示，癫痫组大鼠中的表达最高，具有统计学意义。4. CD68在癫痫组大鼠中最高，具有统计学意义。5. 在旷场实验中，EP组大鼠在中央区域的停留时间延迟，在中央区域移动的距离延长，总移动距离延长，平均速度增加。与EP组大鼠相比，EP+BAY组和EP+TAK组大鼠有不同程度的改善。

结论

在组织水平上，癫痫中TLR4/NF-κB炎症通路的下调可抑制小胶质细胞活化和炎症因子CD68的表达，可抑制过度吞噬，并抑制癫痫的发生和加重，从而改善癫痫发作后的认知和情绪障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/f554289c0d5a/fneur-13-823908-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/63eda04e4fc8/fneur-13-823908-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/57c55be95011/fneur-13-823908-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/81f4cbcfa3dd/fneur-13-823908-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/bb20eca8a88d/fneur-13-823908-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/59143362e22d/fneur-13-823908-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/f554289c0d5a/fneur-13-823908-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/63eda04e4fc8/fneur-13-823908-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/57c55be95011/fneur-13-823908-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/81f4cbcfa3dd/fneur-13-823908-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/bb20eca8a88d/fneur-13-823908-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/59143362e22d/fneur-13-823908-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3147/9046666/f554289c0d5a/fneur-13-823908-g0006.jpg

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