Biochemical, pathological and ultrastructural investigation of whether lamotrigine has neuroprotective efficacy against spinal cord ischemia reperfusion injury

dc.authoridKahveci, Fatih Ozan/0000-0002-6158-501X
dc.authoridGürer, Bora/0000-0003-1500-6184
dc.authoridGökçe, Aysun/0000-0002-4026-6503
dc.contributor.authorKahveci, Fatih Ozan
dc.contributor.authorKahveci, Ramazan
dc.contributor.authorGökçe, Emre Cemal
dc.contributor.authorGökçe, Aysun
dc.contributor.authorKısa, Üçler
dc.contributor.authorSargon, Mustafa Fevzi
dc.contributor.authorFesli, Ramazan
dc.date.accessioned2025-01-21T16:36:11Z
dc.date.available2025-01-21T16:36:11Z
dc.date.issued2021
dc.departmentKırıkkale Üniversitesi
dc.description.abstractIntroduction: Lamotrigine, an anticonvulsant drug with inhibition properties of multi-ion channels, has been shown to be able to attenuates secondary neuronal damage by influencing different pathways. The aim of this study was to look into whether lamotrigine treatment could protect the spinal cord from experimental spinal cord ischemia-reperfusion injury. Materials and methods: Thirty-two rats, eight rats per group, were randomly assigned to the sham group in which only laparotomy was performed, and to the ischemia, methylprednisolone and lamot-rigine groups, where the infrarenal aorta was clamped for thirty minutes to induce spinal cord ischemia-reperfusion injury. Tissue samples belonging to spinal cords were harvested from sacrificed animals twenty-four hours after reperfusion. Tumor necrosis factor-alpha levels, interleukin-1 beta levels, nitric oxide levels, superoxide dismutase activity, catalase activity, glutathione peroxidase activity, malondialde-hyde levels and caspase-3 activity were studied. Light and electron microscopic evaluations were also performed to reveal the pathological alterations. Basso, Beattie, and Bresnahan locomotor scale and the inclined-plane test was used to evaluate neurofunctional status at the beginning of the study and just before the animals were sacrificed. Results: Lamotrigine treatment provided significant improvement in the neurofunctional status by pre -venting the increase in cytokine expression, increased lipid peroxidation and oxidative stress, depletion of antioxidant enzymes activity and increased apoptosis, all of which contributing to spinal cord damage through different paths after ischemia reperfusion injury. Furthermore, lamotrigine treatment has shown improved results concerning the histopathological and ultrastructural scores and the functional tests. Conclusion: These results proposed that lamotrigine may be a useful therapeutic agent to prevent the neuronal damage developing after spinal cord ischemia-reperfusion injury. (c) 2021 Elsevier Ltd. All rights reserved.
dc.identifier.doi10.1016/j.injury.2021.08.004
dc.identifier.endpage2812
dc.identifier.issn0020-1383
dc.identifier.issn1879-0267
dc.identifier.issue10
dc.identifier.pmid34391576
dc.identifier.scopus2-s2.0-85112567539
dc.identifier.scopusqualityQ1
dc.identifier.startpage2803
dc.identifier.urihttps://doi.org/10.1016/j.injury.2021.08.004
dc.identifier.urihttps://hdl.handle.net/20.500.12587/24273
dc.identifier.volume52
dc.identifier.wosWOS:000715855800021
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Sci Ltd
dc.relation.ispartofInjury-International Journal of The Care of The Injured
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241229
dc.subjectAntiinflammatory; antioxidant; apoptosis; lamotrigine; methylprednisolone; neuroprotection; rat; spinal cord; ischemia-reperfusion injury
dc.titleBiochemical, pathological and ultrastructural investigation of whether lamotrigine has neuroprotective efficacy against spinal cord ischemia reperfusion injury
dc.typeArticle

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