title: Activation of Nrf2-ARE signal pathway in hippocampus of amygdala kindling rats.
abstract: Oxidative stress resulting from excessive free-radical release is likely implicated in the initiation and progression of epilepsy. Therefore, antioxidant therapies have received considerable attention in epilepsy treatment. It is well known that the transcription factor NF-E2-related factor (Nrf2) binds to antioxidant response element (ARE) to induce antioxidant and phase II detoxification enzymes under conditions of oxidative stress, which reduces oxidative stress and accumulation of toxic metabolites. However, whether Nrf2-ARE pathway is activated after seizure has not been studied. In the present study, Wistar rats were rapidly kindled in the amygdala. Twenty-four hours after the last seizure, the hippocampus of control, sham and kindled rats were examined for oxidative stress parameters (malondialdehyde and glutathione) by spectrophotometry, the expression of Nrf2, heme oxygenase-1 (HO-1) and NAD(P)H: quinone oxidoreductase-1 (NQO1) were determined using immunohistochemistry, Western blot and real-time fluorescence quantitative polymerase chain reaction (PCR). The results showed that the kindled seizures induced oxidative stress, the expression of Nrf2, HO-1 and NQO1 at protein or gene levels significantly increased in hippocampus after seizure. According to these results, it could be postulated that Nrf2-ARE signal pathway was activated in the hippocampus after seizure.
authors.affiliation: Key Laboratory of Neurology of Hebei Province, the Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050071, PR China.
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Wei-Ping
authors.initials: WP
authors.lastname: Wang
authors.forename: Guo-Liang
authors.initials: GL
authors.lastname: Zhang
authors.forename: Yan-Fen
authors.initials: YF
authors.lastname: Wu
authors.forename: Tao
authors.initials: T
authors.lastname: Xie
authors.forename: Min-Chen
authors.initials: MC
authors.lastname: Kan
authors.forename: Hai-Bo
authors.initials: HB
authors.lastname: Fang
authors.forename: Hong-Chao
authors.initials: HC
authors.lastname: Wang
mesh_terms: D000818:Animals; D061745:Antioxidant Response Elements; D005978:Glutathione / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism*; D007696:Kindling, Neurologic; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000378:metabolism*; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D012640:Seizures / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D051267:NF-E2-Related Factor 2; C495637:Nfe2l2 protein, rat; D008315:Malondialdehyde; D051547:Heme Oxygenase-1; D016660:NAD(P)H Dehydrogenase (Quinone); C507703:NQO1 protein, rat; D005978:Glutathione