Othman, Mohamed SObeidat, Sofian TAleid, Ghada MAl-Bagawi, Amal HFareid, Mohamed AAbdel Hameed, RedaMohamed, Kareem MAbdelfattah, Mohamed SFehaid, AlaaHussein, Manal MAboelnaga, Shimaa M. HAbdel Moneim, Ahmed E2023-02-032023-02-032023-01https://doi.org/ 10.3390/app13021050http://repository.msa.edu.eg/xmlui/handle/123456789/5332We aimed to investigate the potential anticonvulsant effect of green synthetized sele- nium nanoparticles (SeNPs) using Syzygium aromaticum extract (SAE) (SAE-SeNPs) against epileptic seizures and cortical damage induced by pentylenetetrazole (PTZ) injection in rats and its mechanism. A total of 84 rats were divided into six groups; control, PTZ-exposed group, SAE + PTZ-treated group, sodium selenite (Na2SeO3 ) + PTZ-treated group, SAE-SeNPs + PTZ-treated group, and diazepam + PTZ-treated group. SAE-SeNPs significantly increase (p < 0.05) the latency time to seizures and reduce both the seizure duration and death rate, which were enhanced by the PTZ injection. SAE-SeNPs counteracted the PTZ-induced changes in the oxidants and antioxidants. Furthermore, SAE-SeNPs significantly restored (p < 0.05) the pro-inflammatory cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α) to their normal levels and suppressed the activity of the glial fibrillary acidic protein showing their inhibitory effect on the epilepsy-associated inflammation. In addition, SAE-SeNPs significantly reduced (p < 0.05) PTZ-induced cortical cell apoptosis, as revealed by a reduction in the pro-apoptotic Bax and caspase-3 levels, and an elevation of the anti-apoptotic Bcl-2 level. Moreover, SAE-SeNPs significantly modulate (p < 0.05) the PTZ-induced changes in the neuro- transmitter norepinephrine level and acetylcholinesterase enzymatic activity. These data concluded the anticonvulsant activity of SAE-SeNPs via their antioxidant, anti-inflammatory, and anti-apoptotic effects, along with their ability to modulate neurotransmitters.en-USSyzygium aromaticum;selenium nanoparticles;epilepsy; oxidant;neuroinflammation;apoptosis;neurotransmitter;cerebral cortexArticlehttps://doi.org/ 10.3390/app13021050