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Ibuprofen Exerts Antiepileptic and Neuroprotective Effects in the Rat Model of Pentylenetetrazol-Induced Epilepsy via the COX-2/NLRP3/IL-18 Pathway.
Neurochemical Research ( IF 3.7 ) Pub Date : 2020-08-13 , DOI: 10.1007/s11064-020-03109-9
Rui Liu 1 , Shuhua Wu 2 , Chong Guo 1 , Zhongbo Hu 1 , Jiangtao Peng 1 , Ke Guo 1 , Xinfan Zhang 1 , Jianmin Li 1
Affiliation  

Epilepsy is one of the most common diseases of the central nervous system. Recent studies have shown that a variety of inflammatory mediators play a key role in the pathogenesis of the disease. Ibuprofen (IBP) is a well-known anti-inflammatory agent that reduces the neuroinflammatory response and neuronal damage. In this study, we examined the effect of IBP in a rat model of pentylenetetrazol (PTZ)-induced chronic epilepsy. PTZ injection was given a total of 15 times on alternate days (over a period of 29 days) to induce epilepsy. The effects of IBP were evaluated by behavioral observation, EEG recording, Nissl staining, immunohistochemistry, Western blot analysis, and electrophysiological recording. The results showed that IBP alone affected the expression of cyclooxygenase-2 (COX-2) and neuronal excitability but did not cause epilepsy. IBP reduced seizure scores in the PTZ-treated rats, and it minimized the loss of hippocampal neurons. In addition, IBP decreased the secretion of COX-2, inhibited the activation of the NOD-like receptor 3 inflammasome, and reduced the secretion of the inflammatory cytokine interleukin-18. Furthermore, the results of whole-cell patch-clamp revealed that IBP affected action potential properties, including frequency, latency and duration in epileptic rats, suggesting that it may impact neuronal excitability. These effects of IBP may underlie its antiepileptic and neuroprotective actions.



中文翻译:

布洛芬在戊四氮诱导的癫痫大鼠模型中通过COX-2 / NLRP3 / IL-18途径发挥抗癫痫和神经保护作用。

癫痫病是中枢神经系统最常见的疾病之一。最近的研究表明,多种炎性介质在该疾病的发病机理中起关键作用。布洛芬(IBP)是一种众所周知的抗炎药,可减少神经炎症反应和神经元损伤。在这项研究中,我们检查了IBP在戊四氮(PTZ)诱发的慢性癫痫大鼠模型中的作用。隔天(29天之内)共进行15次PTZ注射以诱发癫痫病。通过行为观察,EEG记录,Nissl染色,免疫组织化学,Western印迹分析和电生理记录来评估IBP的作用。结果表明,IBP单独影响环氧合酶2(COX-2)的表达和神经元兴奋性,但不会引起癫痫。IBP降低了经PTZ治疗的大鼠的癫痫发作评分,并使海马神经元的损失最小化。此外,IBP减少了COX-2的分泌,抑制了NOD样受体3炎性小体的活化,并减少了炎性细胞因子白介素18的分泌。此外,全细胞膜片钳的结果显示,IBP影响癫痫大鼠的动作电位特性,包括频率,潜伏期和持续时间,表明它可能影响神经元兴奋性。IBP的这些作用可能是其抗癫痫和神经保护作用的基础。并减少了炎性细胞因子白介素18的分泌。此外,全细胞膜片钳的结果显示,IBP影响癫痫大鼠的动作电位特性,包括频率,潜伏期和持续时间,表明它可能影响神经元兴奋性。IBP的这些作用可能是其抗癫痫和神经保护作用的基础。并减少了炎性细胞因子白介素18的分泌。此外,全细胞膜片钳的结果显示,IBP影响癫痫大鼠的动作电位特性,包括频率,潜伏期和持续时间,表明它可能影响神经元兴奋性。IBP的这些作用可能是其抗癫痫和神经保护作用的基础。

更新日期:2020-09-23
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