| 杨萍
，黄惠勇
，李丰.NLRP3对匹罗卡品致癫痫大鼠模型海马齿状回的作用[J].神经损伤功能重建,2020,15(5):271-273 |
| NLRP3对匹罗卡品致癫痫大鼠模型海马齿状回的作用 |
| Effect of NLRP3 on Hippocampal Dentate Gyrus in Pilocarpine-Induced Rat Epilepsy Model |
| |
| DOI： |
| 中文关键词: 癫痫 NLRP3 Caspase-1 炎症反应 |
| 英文关键词: epilepsy NLRP3 Caspase-1 inflammation |
| 基金项目:国家自然科学基
金（No. 81603512，
81874429）；
湖南省卫生计生
委科研课题（No.
20180364）；
湖南省卫生计生
委科研课题（No.2
0200009)；
湖南省教育厅科
学研究项目（No.1 9B440)；
湖南省中医药科
研计划项目（No.
201818） |
|
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| 中文摘要: |
| 目的：探讨NLRP3在匹罗卡品致癫痫大鼠模型中海马齿状回的表达及作用。方法：大鼠64只，随机选
取12只为对照组，其余大鼠建立氯化锂-匹罗卡品癫痫模型，造模成功后随机分为1 d、7 d、14 d、28 d组，每组
12只。ELISA检测大鼠血清IL-1β、TNF含量；免疫组化、RT-PCR检测大鼠海马组织齿状回NLRP3、Caspase-1
在癫痫造模后不同时间点的表达水平。结果：7 d、14 d、28 d 组血清中 IL-1β、TNF 的含量较对照组高（P< 0.01），且28 d组最高，高于其他组（P<0.01）；7 d、14 d、28 d组大鼠海马组织齿状回NLRP3、Caspase-1平均光
密度，海马组织NLRP3、Caspase-1 mRNA表达均高于对照组（P<0.01），且28 d组最高，高于其他组（P<0.01）。
结论：在慢性自发性癫痫形成过程中，NLRP3、Caspase-1在大鼠模型海马齿状回中表达升高，可能与激活炎症
反应有关。 |
| 英文摘要: |
| To explore the effect of NLRP3 on the hippocampal dentate gyrus in the
pilocarpine-induced rat epilepsy model. Methods: Twelve rats were randomly selected from 64 adult SD rats as
controls, and the others were induced by lithium-pilocarpine to create the epilepsy model. After model
establishment, the rats were randomly divided into the 1 d, 7 d, 14 d, and 28 d groups (n=12 per group). The serum
levels of IL-1β and TNF were detected with ELISA. The expression of NLRP3 and Caspase-1 in the hippocampal
dentate gyrus was measured with immunohistochemistry and RT-PCR. Results: The serum levels of IL-1β and
TNF in the 7 d, 14 d, and 28 d group rats were higher than those in control group rats (P<0.01), and that of the 28
d group was highest among all groups (P<0.01). The average optical density and mRNA expression of NLRP3 and
Caspase-1 in the hippocampal dentate gyrus of 7 d, 14 d, and 28 d group rats were higher than those in control
group rats (P<0.01), and that of the 28 d group was highest among all groups (P<0.01). Conclusion: Expression
of NLRP3 and Caspase-1 increased in the hippocampal dentate gyrus of pilocarpine-induced model rats during the
progression of chronic spontaneous epilepsy. This may be associated with activation of the inflammatory response. |
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