Abstract
Epilepsy is a common neurological disorder which affects patients physically and mentally and causes a real burden for the patient, family and society both medically and economically. Currently, more than one-third of epilepsy patients are still under unsatisfied control, even with new anticonvulsants. Other measures may be added to those with drug-resistant epilepsy. Excessive neuronal synchronization is the hallmark of epileptic activity and prolonged epileptic discharges such as in status epilepticus can lead to various cellular events and result in neuronal damage or death. Unbalanced oxidative status is one of the early cellular events and a critical factor to determine the fate of neurons in epilepsy. To counteract excessive oxidative damage through exogenous antioxidant supplements or induction of endogenous antioxidative capability may be a reasonable approach for current anticonvulsant therapy. In this article, we will introduce the critical roles of oxidative stress and further discuss the potential use of antioxidants in this devastating disease.
Highlights
Epilepsy is a common neurological disorder and estimated with a prevalence of 0.5–1.5% in the general population varying between developed countries and developing countries [1,2,3]
Antiepileptic drug or anticonvulsants is a standard treatment for patients with epilepsy, more than one-third of patients remain in poor control of seizure frequency, the so-called drug-resistant epilepsy even with the several new antiepileptic drugs used in recent decades
Mounting evidence revealed the success of antioxidants treatment in status epilepticus in pre-clinical studies as summarized in Table 1, the difficulty of translation into clinical practice is obvious from the information of CliniclTrials.gov
Summary
Epilepsy is a common neurological disorder and estimated with a prevalence of 0.5–1.5% in the general population varying between developed countries and developing countries [1,2,3]. We have demonstrated that the downregulation of sirtuin can reduce PGC-1α expression, impair mitochondrial biogenesis, augment Complex I dysfunction, heighten the extent of oxidized proteins, increase caspase-3 expression, and promote neuronal cell damage in the hippocampus in kainic acid-induced status epilepticus [96]. It was shown that sirtuin, a major mitochondria NAD+-dependent deacetylase, through regulating manganese SOD to lessen excessive oxidative stress from mitochondria can reduce neuronal damage in hippocampal cells after status epilepticus [98] With these studies, it is noteworthy to further explore the vital role of the sirtuin family in seizure disorders, and this may open an avenue to develop innovative therapy in epilepsy in the future. We will further discuss the significance of antioxidants used in status epilepticus
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