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黑种草醌对癫痫持续状态模型中锂-匹鲁卡品诱导的惊厥活性的保护作用。

Protective Effects of Thymoquinone Against Convulsant Activity Induced by Lithium-Pilocarpine in a model of Status Epilepticus.

作者信息

Shao Yiye, Feng Yonghao, Xie Yangmei, Luo Qiong, Chen Long, Li Bing, Chen Yinghui

机构信息

Department of Neurology, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 201508, China.

Center Laboratory, Jinshan Hospital, Fudan University, 1508 Longhang Road, Shanghai, 200040, China.

出版信息

Neurochem Res. 2016 Dec;41(12):3399-3406. doi: 10.1007/s11064-016-2074-y. Epub 2016 Oct 18.

DOI:10.1007/s11064-016-2074-y
PMID:27752802
Abstract

Inflammation plays a pivotal role in status epilepticus (SE). Thymoquinone (TQ) is a bioactive monomer extracted from black seed (Nigella sativa) oil, which has anti-inflammatory properties in the context of various diseases. This study explored the protective effects of TQ in SE and used a lithium-pilocarpine model of SE to investigate the underlying mechanism, which was related to inflammation mediated by the NF-κB signaling pathway. In the present study, latency to SE increased in the TQ-pretreated group compared with the SE group, and the incidence of SE was significantly reduced. The seizure severity score measured on the Racine scale was significantly decreased in the TQ group compared with the SE group. Moreover, the results of the behavioral tests suggested that TQ may also have a protective effect on learning and memory functions. Finally, we further investigated the protective mechanism of TQ. The results showed that TQ-pretreatment significantly downregulated the protein levels of COX-2 and TNF-α in the brain, in a manner mediated by the NF-κB signaling pathway. These findings demonstrate that TQ attenuates convulsant activity via an anti- inflammation signaling pathway in a model of SE.

摘要

炎症在癫痫持续状态(SE)中起关键作用。百里醌(TQ)是从黑种草籽油中提取的一种生物活性单体,在多种疾病中具有抗炎特性。本研究探讨了TQ对SE的保护作用,并使用SE的锂-匹罗卡品模型研究其潜在机制,该机制与核因子κB(NF-κB)信号通路介导的炎症有关。在本研究中,与SE组相比,TQ预处理组的SE潜伏期延长,SE发生率显著降低。与SE组相比,TQ组根据拉辛量表测得的癫痫严重程度评分显著降低。此外,行为测试结果表明,TQ可能对学习和记忆功能也有保护作用。最后,我们进一步研究了TQ的保护机制。结果显示,TQ预处理通过NF-κB信号通路显著下调大脑中环氧合酶-2(COX-2)和肿瘤坏死因子-α(TNF-α)的蛋白水平。这些发现表明,在SE模型中,TQ通过抗炎信号通路减弱惊厥活性。

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