Lateef Mohiuddin Khan, Shahid Karim

Abstract

Background: Nigella sativa (NS) has antioxidant and neuroprotective effects. Its concurrent use with AEDs could be a promising health strategy to prevent the damaging effect on neuronal cells during the episodes of seizures in addition to enhancing therapeutic effects and diminishing the adverse drug reactions of AEDs. Purpose: To provide the pragmatic perception of utilizing TQ as an adjuvant in antiepileptic therapies to potentiate their actions. Methods: The study utilizes systematic reviews on publications of previous studies obtained from scholarly journal databases including PubMed, Medline, Ebsco Host, Google Scholar, and Cochrane. The study utilizes secondary information obtained from health organizations using filters and keywords to sustain information relevancy. The use of search keywords and filters limits the study to relevant peer-reviewed journals. The study utilizes information retrieved from in vivo, in vitro and clinical studies captured in the peer-reviewed journals on “thymoquinone and epilepsy”, “thymoquinone and neuroprotection” “Nigella Sativa and epilepsy, “thymoquinone and AEDs” “model of epilepsy and thymoquinone”. Results: TQ was demonstrated to inhibit apoptosis and neuronal degeneration in the cerebral cortex. Furthermore, Nigella sativa oil and its active ingredient TQ protects brain tissue against radiation-induced nitrosative stress, TQ plays a crucial protective activity in the rat hippocampus and cortical neurons against Aββ1-42 and thus, it may be a promising agent for the treatment of Alzheimer’s disease. An interesting series of studies also reported that TQ has shown antiepileptic effects. Akhondian et al. reported that orally administered TQ reduces intractable pediatric seizures. Also, Hosseinzadeh et al., showed that TQ administered intracerebroventricularly, for epileptiform activity induced by using pentylenetetrazole (PTZ) in rats, prolonged the latency to first seizure, and decreased seizure count and the periods of tonic-clonic seizure in a dose-dependent manner. In another study, orally administered TQ prolonged the first seizure latency, decreased seizure count, and eliminated lethality in PTZ-induced epilepsy. TQ has a protective and inhibitory effect on a penicillin epilepsy model, as with the other experimental epilepsy models. Conclusion: The current approach to AED discovery is effective for identifying drugs that are useful for the symptomatic treatment of seizures. However, such an approach cannot be adequate to develop therapies for preventing and modifying the development of epilepsy in a susceptible person. Undoubtedly, TQ is demonstrated as an ideal adjuvant to antiepileptic therapies by potentiating their actions and retreating their adverse effects.