Unveiling the Protective Potential of Sugammadex against PTZ-Induced Epileptic Seizures in Mice: A Comprehensive Study on Oxidative Stress, Apoptosis, and Autophagy

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dc.contributor.authorKarademir, Mustafa
dc.contributor.authorOzturk, Aysegul
dc.contributor.authorYulak, Fatih
dc.contributor.authorOzkaraca, Mustafa
dc.contributor.authorTaskiran, Ahmet Sevki
dc.date.accessioned2024-10-26T18:04:07Z
dc.date.available2024-10-26T18:04:07Z
dc.date.issued2024
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractSugammadex (SUG) is a modified gamma-cyclodextrin molecule used in patients under general anesthesia to reverse the effects of neuromuscular blocking agents. Besides, recent studies have shown that SUG positively affects the nervous system. However, its effect on seizures is still unclear. The current study aimed to examine the effects of SUG on pentylenetetrazole (PTZ)-induced epileptic seizures in mice. The mice were randomly divided into four groups. Group 1 was controlled, group 2 was administered saline (1 mL/kg serum physiologic), and Groups 3 and 4 were administered Sugammadex (150 and 300 mg/kg). Pentylenetetrazole (60 mg/kg) was given to induce seizures 30 min after saline or drug administration except for the control group. Total oxidant status (TOS) and total antioxidant status (TAS) levels in the hippocampus and cortex were measured using a commercial kit. 8-hydroxydeoxyguanosine (8-OHdG), 4-hydroxynonenal (4-HNE), 3,3 dityrosine, caspase-3, apoptosis-inducing factor (AIF), and light chain 3 (LC3B) levels in the hippocampal CA1 region and cortex after seizures were evaluated immunohistochemical staining. SUG reduced seizure stages and increased epileptic seizure onset times. Moreover, it decreased TOS levels and increased TAS levels in the hippocampus and cortex. Besides, after seizures, it reduced 4-HNE, 3,3 dityrosandine, caspase-3, and LC3B immunohistochemical scores in the hippocampal CA1 region and cortex. SUG has protective effects on pentylenetetrazole-induced seizures in mice, alleviating seizures, oxidative stress, apoptosis, and autophagy. The anticonvulsant mechanism of SUG may be related to the inhibition of the oxidative stress pathway.
dc.identifier.doi10.1134/S1819712424020181
dc.identifier.endpage347
dc.identifier.issn1819-7124
dc.identifier.issn1819-7132
dc.identifier.issue2
dc.identifier.startpage338
dc.identifier.urihttps://doi.org/10.1134/S1819712424020181
dc.identifier.urihttps://hdl.handle.net/20.500.12418/28760
dc.identifier.volume18
dc.identifier.wosWOS:001233389200013
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.language.isoen
dc.publisherMaik Nauka/Interperiodica/Springer
dc.relation.ispartofNeurochemical Journal
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectseizure
dc.subjectpentylenetetrazole
dc.subjectsugammadex
dc.subjectoxidative stress
dc.subjectapoptosis
dc.subjectautophagy
dc.titleUnveiling the Protective Potential of Sugammadex against PTZ-Induced Epileptic Seizures in Mice: A Comprehensive Study on Oxidative Stress, Apoptosis, and Autophagy
dc.typeArticle

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