title: Thymoquinone Attenuates Brain Injury via an Anti-oxidative Pathway in a Status Epilepticus Rat Model.
abstract: OBJECTIVE
  Status epilepticus (SE) results in the generation of reactive oxygen species (ROS), which contribute to seizure-induced brain injury. It is well known that oxidative stress plays a pivotal role in status epilepticus (SE). Thymoquinone (TQ) is a bioactive monomer extracted from black cumin (Nigella sativa) seed oil that has anti-inflammatory, anti-cancer, and antioxidant activity in various diseases. This study evaluated the protective effects of TQ on brain injury in a lithium-pilocarpine rat model of SE and investigated the underlying mechanism related to antioxidative pathway.
  
  
  METHODS
  Electroencephalogram and Racine scale were used to value seizure severity. Passive-avoidance test was used to determine learning and memory function. Moreover, anti-oxidative activity of TQ was observed using Western blot and super oxide dismutase (SOD) activity assay.
  
  
  RESULTS
  Latency to SE increased in the TQ-pretreated group compared with rats in the model group, while the total power was significantly lower. Seizure severity measured on the Racine scale was significantly lower in the TQ group compared with the model group. Results of behavioral experiments suggest that TQ may also have a protective effect on learning and memory function. Investigation of the protective mechanism of TQ showed that TQ-pretreatment significantly increased the expression of Nrf2, HO-1 proteins and SOD in the hippocampus.
  
  
  CONCLUSIONS
  These findings showed that TQ attenuated brain injury induced by SE via an anti-oxidative pathway.
authors.affiliation: Department of Neurology, Jinshan Hospital, Fudan University, Shanghai 201508, China.
authors.forename: Yi-Ye
authors.initials: YY
authors.lastname: Shao
authors.affiliation: Center Laboratory, Jinshan Hospital, Fudan University, Shanghai 200040, China.
authors.forename: Bing
authors.initials: B
authors.lastname: Li
authors.affiliation: Department of Neurology, Jinshan Hospital, Fudan University, Shanghai 201508, China.
authors.forename: Yong-Mei
authors.initials: YM
authors.lastname: Huang
authors.affiliation: Department of Neurology, Jinshan Hospital, Fudan University, Shanghai 201508, China.
authors.forename: Qiong
authors.initials: Q
authors.lastname: Luo
authors.affiliation: Department of Neurology, Jinshan Hospital, Fudan University, Shanghai 201508, China.
authors.forename: Yang-Mei
authors.initials: YM
authors.lastname: Xie
authors.affiliation: Department of Neurology, Jinshan Hospital, Fudan University, Shanghai 201508, China.
authors.forename: Ying-Hui
authors.initials: YH
authors.lastname: Chen
keywords: Nrf2; brain injury; oxidative stress; status epilepticus; thymoquinone