4.6 Article

Green Synthetized Selenium Nanoparticles Using Syzygium aromaticum (Clove) Extract Reduce Pentylenetetrazol-Induced Epilepsy and Associated Cortical Damage in Rats

Journal

APPLIED SCIENCES-BASEL
Volume 13, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/app13021050

Keywords

Syzygium aromaticum; selenium nanoparticles; epilepsy; oxidant; neuroinflammation; apoptosis; neurotransmitter; cerebral cortex

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The study aimed to explore the potential anticonvulsant effect of green synthetized selenium nanoparticles (SeNPs) using Syzygium aromaticum extract (SAE) (SAE-SeNPs) on epileptic seizures and cortical damage induced by pentylenetetrazole (PTZ) injection in rats, as well as its mechanism. SAE-SeNPs demonstrated a significant increase in seizure latency time, reduction in seizure duration and death rate, counteracted PTZ-induced changes in oxidants and antioxidants, restored pro-inflammatory cytokine levels, and suppressed glial fibrillary acidic protein activity. Furthermore, SAE-SeNPs reduced PTZ-induced cortical cell apoptosis and modulated neurotransmitter levels. The study concludes that SAE-SeNPs exhibit anticonvulsant activity through antioxidant, anti-inflammatory, and anti-apoptotic effects, and modulation of neurotransmitters.
We aimed to investigate the potential anticonvulsant effect of green synthetized selenium 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-1 beta, interleukin-6, and tumor necrosis factor-alpha) 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 neurotransmitter 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.

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