Şahin S.Gürgen S.G.Yazar U.İnce İ.Kamaşak T.Acar Arslan E.Diler Durgut B.Dilber B.Cansu A.2024-07-222024-07-22201909201211http://akademikarsiv.cbu.edu.tr:4000/handle/123456789/14710Objectives: The hippocampus is susceptible to damage in patients with epilepsy and in animals with seizures caused by excitotoxic agents. The effect of vitamin D on hippocampal apoptosis related with seizures has not been reported. However, epileptic patients have an increased risk of hypovitaminosis D which is most likely due to the effects of antiepileptic drugs. Therefore, in this study, it was aimed to evaluate the effects of vitamin D on hippocampal apoptosis related with seizures by using pentylenetetrazol (PTZ) and kainic acid (KA) in rats. Methods: Male Sprague Dawley rats, aged 5.5 weeks, were randomly divided into six groups: control, vitamin D, PTZ, KA, PTZ + vitamin D and KA + vitamin D groups. The groups that received vitamin D were given 500 IU/kg of vitamin D daily for two weeks in addition to a standard diet. At the end of this period, PTZ and KA were applied to trigger seizures in the rats in the seizure groups. 24 h after the administration of PTZ and KA, the rats were decapitated. In the hippocampal region, apoptosis was assessed by TUNEL and brain-derived neurotrophic factor (BDNF), Bax, caspase-3 and c-fos activation were evaluated by immunohistochemical method. Results: BDNF level increased while c-fos, Bax and caspase-3 levels decreased (p < 0.0001, in all) in the hippocampal neurons of the groups that were pre-treated with vitamin D before the administration of PTZ and KA, in comparison with the PTZ and KA groups. Vitamin D significantly decreased the number of apoptotic cells in these rats in comparison with the PTZ and KA groups (p < 0.0001). Conclusion: This study indicates that vitamin D has neuroprotective effects on hippocampal apoptosis induced by PTZ and KA in rats. With this study it is suggested that keeping vitamin D levels within normal limits may be beneficial for patients with epilepsy, especially children. © 2018 Elsevier B.V.EnglishAnimalsApoptosisbcl-2-Associated X ProteinBrain-Derived Neurotrophic FactorCaspase 3ConvulsantsDisease Models, AnimalHippocampusIn Situ Nick-End LabelingKainic AcidMaleNeuronsNeuroprotective AgentsPentylenetetrazoleProto-Oncogene Proteins c-fosRatsRats, Sprague-DawleySeizuresVitamin Dbrain derived neurotrophic factorcaspase 3devit 3protein Baxvitamin Dbrain derived neurotrophic factorcaspase 3convulsant agentkainic acidneuroprotective agentpentetrazoleprotein Baxprotein c fosvitamin Danimal experimentanimal modelanimal tissueapoptosisArticlecontrolled studydrug efficacyenzyme activationhippocampal CA3 regionhippocampusimmunohistochemistrykainic acid-induced seizuremaleneuroprotectionnonhumanoutcome assessmentpentylenetetrazole-induced seizurepriority journalprotein expressionrandomized controlled trialratTUNEL assayanimalapoptosischemically induceddisease modeldrug effecthippocampusmetabolismnerve cellpathologyseizureSprague Dawley ratArticle10.1016/j.eplepsyres.2018.12.005