Abstract

Epilepsy is a common brain disorder characterized by a persistent propensity to produce spontaneous seizures. The means by which epilepsy develops are still a mystery. In both human and experimental temporal lobe epilepsy, prolonged seizures cause significant neuroinflammatory responses, which are thought to mediate epileptogenesis. At the moment, there is a lot of evidence that anti-inflammatory treatments might be a good alternative to medication, especially if antiepileptic drugs don't work. By reducing the calming exercises of epoxyeicosatrienoic acids (EETs), dissolvable epoxide hydrolase (sEH) has been viewed as an expected remedial objective for epileptic seizures. The physiological functions of EETs-sEH metabolism in the central nervous system, the connection of the EET-sEH pathway to neuroinflammation and neuromodulation, and the relevance of neuro inflammarion to the pathophysiology of epilepsy are all examined in this review. The significance of sEH inhibition in regulating inflammatory responses and abnormal hyperexcitability associated with epilepsy has been defined by a number of recent studies. Even though there are some differences between different experimental models or between pharmacological inhibition and genetic deletion of sEH, the fact that sEH is involved in the onset and progression of epilepsy suggests that sEH could be a promising therapeutic target.