Carmona-Aparicio Liliana, Pérez-Cruz Claudia, Zavala-Tecuapetla Cecilia, Granados-Rojas Leticia, Rivera-Espinosa Liliana, Montesinos-Correa Hortencia, Hernández-Damián Jacqueline, Pedraza-Chaverri José, Sampieri Aristides, Coballase-Urrutia Elvia, Cárdenas-Rodríguez Noemí
Laboratory of Neurochemistry (Neurosciences), National Institute of Pediatrics, D.F. 04530, Mexico.
Laboratory of Neuroplasticity and Neurodegeneration, Cinvestav, D.F. 07360, Mexico.
Int J Mol Sci. 2015 Aug 7;16(8):18348-67. doi: 10.3390/ijms160818348.
Oxidative stress is a biochemical state of imbalance in the production of reactive oxygen and nitrogen species and antioxidant defenses. It is involved in the physiopathology of degenerative and chronic neuronal disorders, such as epilepsy. Experimental evidence in humans and animals support the involvement of oxidative stress before and after seizures. In the past few years, research has increasingly focused on the molecular pathways of this process, such as that involving transcription factor nuclear factor E2-related factor 2 (Nrf2), which plays a central role in the regulation of antioxidant response elements (ARE) and modulates cellular redox status. The aim of this review is to present experimental evidence on the role of Nrf2 in this neurological disorder and to further determine the therapeutic impact of Nrf2 in epilepsy.
氧化应激是活性氧和氮物种产生与抗氧化防御之间失衡的生化状态。它参与退行性和慢性神经疾病(如癫痫)的生理病理学过程。人和动物的实验证据支持癫痫发作前后氧化应激的参与。在过去几年中,研究越来越关注这一过程的分子途径,例如涉及转录因子核因子E2相关因子2(Nrf2)的途径,Nrf2在抗氧化反应元件(ARE)的调节中起核心作用,并调节细胞氧化还原状态。本综述的目的是提供关于Nrf2在这种神经疾病中作用的实验证据,并进一步确定Nrf2对癫痫的治疗影响。