癫痫是神经系统常见病，治疗以药物为主。抗痫药物主要抑制症状，难以预防癫痫的发生。近年研究表明脑内炎症可能在癫痫发生中起到决定性作用。阿曼托双黄酮广泛存在于许多药用植物内，具有抗炎、抗氧化、抗凋亡等活性。课题组前期研究显示：阿曼托双黄酮显著缩短致痫小鼠癫痫发作持续时间，减少海马神经元缺失，降低NF-κB p65表达。显示阿曼托双黄酮有可能通过抗炎、抗氧化作用预防癫痫发生。本研究拟建立匹罗卡品致痫模型，应用视频脑电、水迷宫和避暗实验观察阿曼托双黄酮对致痫大鼠自发性癫痫发作及认知功能的影响；应用ELISA、免疫组化、病理学等技术检测海马氧化应激及神经元变性、坏死、凋亡情况，明确阿曼托双黄酮在癫痫发生时的神经保护作用；采用组织学、分子生物学等技术检测炎性相关因子、AchE、GABAA R亚基α1、γ2、δ等，探讨阿曼托双黄酮抗癫痫发生机制，并进一步阐明炎症与癫痫发生的关系，为抗痫新药研发开拓思路。

Epilepsy, one of the most common neurological disorders, is characterized by recurrent, usually unprovoked, epileptic seizures, and followed with the cognitive, psychosocial, and social consequences. The available therapy against epilepsy is only symptomatic and often ineffective. The most important challenge is to prevent the process of epileptogenesis, not merely to treat its symptoms. At present, there is no anti-epileptic drug that performs this function. Thus, there is an urgent need to develop novel therapeutic interventions that are disease modifying-therapies that either completely or partially prevent the emergence of spontaneous recurrent seizures. Epileptogenesis is a process in which various insults ( such as brain insult, stroke, SE, the inflammatin in brain, etc.) induce brain to generate a cascade event, enhance the susceptivity of seizure and generate spontaneous recurrent seizures. In the last decade, Clinical and experimental evidence substantiate that brain inflammation is a common substrate in epilepsies of different etiologies. The use of antiinflammatory drugs in epilepsy has been invoked as a promising therapeutic strategy. In recent years, the research on medicinal plants is a hot point. Amentoflavone, a biflavonoid, widely distributed in plant kingdom.it has been found to possess anti-inflammatory, antioxidative, anti-apoptosis, and neuroprotective effects. Based on the above, it is reasonable to hypothesize that Amentoflavone may play a neuro-protective role in epileptic model and may have the anti-epileptogensis role. Our previous research found that amentoflavone significantly prolonged the latency of seizure attacks and reduced the amplitude and duration of epileptiform burst discharges induced by injection of intraperitoneal Pilocarpine. In addition, Amentoflavone significantly increased the survived neurons of hippocampal CA1, reduced apoptotic of neurons,and inhibited NF-κB p65 expression. On the basis of these considerations, we design the following experiment to investigate antiepileptogenic effects of amentoflavone in the pilocarpine-induced rat model.Spontaneous recurrent seizures (SRSs) were investigated by video-EEG monitoring during the entire procedure. Cognitive function was evaluated by the passive avoidance test and Morris water maze test. Brain tissue damage, oxidative stress parameters, inflammatory cytokines, mossy fiber sprouting, impact to AchE, and GABAA receptors subunit (α1, γ2, and δ) will be assessed by histology and immunohistochemistry. We hope to found new therapies to modify the epileptic process.