dc.contributor.author | Erdogan M.A. | |
dc.contributor.author | Yigitturk G. | |
dc.contributor.author | Erbas O. | |
dc.contributor.author | Taskıran D. | |
dc.date.accessioned | 2024-02-04T13:30:09Z | |
dc.date.available | 2024-02-04T13:30:09Z | |
dc.date.issued | 2022 | |
dc.identifier.issn | 01480545 | |
dc.identifier.uri | https://doi.org/10.1080/01480545.2021.1914464 | |
dc.identifier.uri | http://hdl.handle.net/11446/4853 | |
dc.description.abstract | Aim: Although the most common age-related neurodegenerative disease defined by memory loss is Alzheimer's disease (AD), only symptomatic therapies are present. A complex pathway for the AD pathogenesis that includes an increase in inflammation has recently been suggested. Since in previous animal experiments dexpanthenol has anti-inflammatory and neuroprotective activities, effects and role of dexpanthenol in an intracerebroventricular (ICV)-streptozotocin (STZ) induced sporadic-AD(memory impairment) animal model have been examined. Design and methods: In total, 18 adult sprague-dawley rats were classified into 3 groups; control (n = 6), STZ + Saline (n = 6) and STZ + Dexpanthenol (n = 6). Twelve AD-induced rats through STZ-injection (3 mg/kg) into both lateral ventricles via stereotaxy were separated into two groups five days after STZ administration: one of these groups was treated with dexpanthenol (1000 mg/kg/day, i.p.) for 3 weeks and the other with saline. A passive avoidance learning (PAL) test was used after treatment, followed by brain tissue extraction in all subjects. Brain levels of tumor necrosis factor-alpha (TNF-?) and choline acetyl transferase (ChAT) were measured and Cresyl violet staining was used to count neurons in cornu ammonis-1 (CA1) and cornu ammonis-3 (CA3). Results: It was observed that ICV-STZ significantly shortened PAL latency, increased levels of TNF-? in brain, decreased activity of ChAT in brain, and number of hippocampal neurons. However, dexpanthenol significantly reduced all of those STZ-induced harmful effects. Conclusion: Dexpanthenol significantly prevented the memory deficit induced by ICV-STZ through mitigating neuronal loss in hippocampus, cholinergic deficiency and neuroinflammation in rats. These findings suggest that dexpanthenol may be beneficial for treating memory impairment. © 2021 Informa UK Limited, trading as Taylor & Francis Group. | en_US |
dc.description.sponsorship | This study did not recieve any funding. | en_US |
dc.language.iso | eng | en_US |
dc.publisher | Taylor and Francis Ltd. | en_US |
dc.relation.ispartof | Drug and Chemical Toxicology | en_US |
dc.identifier.doi | 10.1080/01480545.2021.1914464 | |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | Alzheimer’s disease | en_US |
dc.subject | dexpanthenol | en_US |
dc.subject | hippocampus | en_US |
dc.subject | memory impairment | en_US |
dc.subject | neuroprotection | en_US |
dc.subject | streptozotocin | en_US |
dc.subject | alfazyne | en_US |
dc.subject | choline acetyltransferase | en_US |
dc.subject | dexpanthenol | en_US |
dc.subject | ketamine | en_US |
dc.subject | retinol | en_US |
dc.subject | streptozocin | en_US |
dc.subject | tumor necrosis factor | en_US |
dc.subject | xylazine | en_US |
dc.subject | choline acetyltransferase | en_US |
dc.subject | dexpanthenol | en_US |
dc.subject | neuroprotective agent | en_US |
dc.subject | pantothenic acid | en_US |
dc.subject | streptozocin | en_US |
dc.subject | tumor necrosis factor | en_US |
dc.subject | adult | en_US |
dc.subject | Alzheimer disease | en_US |
dc.subject | animal cell | en_US |
dc.subject | animal experiment | en_US |
dc.subject | animal model | en_US |
dc.subject | animal tissue | en_US |
dc.subject | antiinflammatory activity | en_US |
dc.subject | Article | en_US |
dc.subject | biochemical analysis | en_US |
dc.subject | brain lateral ventricle | en_US |
dc.subject | brain level | en_US |
dc.subject | brain tissue | en_US |
dc.subject | controlled study | en_US |
dc.subject | enzyme activity | en_US |
dc.subject | hippocampal CA1 region | en_US |
dc.subject | hippocampal CA3 region | en_US |
dc.subject | histopathology | en_US |
dc.subject | latent period | en_US |
dc.subject | learning | en_US |
dc.subject | male | en_US |
dc.subject | memory disorder | en_US |
dc.subject | nerve cell | en_US |
dc.subject | nerve injury | en_US |
dc.subject | nervous system inflammation | en_US |
dc.subject | neuroprotection | en_US |
dc.subject | nonhuman | en_US |
dc.subject | passive avoidance | en_US |
dc.subject | rat | en_US |
dc.subject | stereotactic procedure | en_US |
dc.subject | animal | en_US |
dc.subject | degenerative disease | en_US |
dc.subject | disease model | en_US |
dc.subject | hippocampus | en_US |
dc.subject | human | en_US |
dc.subject | maze test | en_US |
dc.subject | memory disorder | en_US |
dc.subject | metabolism | en_US |
dc.subject | pathology | en_US |
dc.subject | Sprague Dawley rat | en_US |
dc.subject | Wistar rat | en_US |
dc.subject | Alzheimer Disease | en_US |
dc.subject | Animals | en_US |
dc.subject | Choline O-Acetyltransferase | en_US |
dc.subject | Disease Models, Animal | en_US |
dc.subject | Hippocampus | en_US |
dc.subject | Humans | en_US |
dc.subject | Maze Learning | en_US |
dc.subject | Memory Disorders | en_US |
dc.subject | Neurodegenerative Diseases | en_US |
dc.subject | Neurons | en_US |
dc.subject | Neuroprotective Agents | en_US |
dc.subject | Pantothenic Acid | en_US |
dc.subject | Rats | en_US |
dc.subject | Rats, Sprague-Dawley | en_US |
dc.subject | Rats, Wistar | en_US |
dc.subject | Streptozocin | en_US |
dc.subject | Tumor Necrosis Factor-alpha | en_US |
dc.title | Neuroprotective effects of dexpanthenol on streptozotocin-induced neuronal damage in rats | en_US |
dc.type | article | en_US |
dc.department | DBÜ | en_US |
dc.identifier.issue | 5 | en_US |
dc.identifier.volume | 45 | en_US |
dc.identifier.startpage | 2160 | en_US |
dc.identifier.endpage | 2168 | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.department-temp | Erdogan, M.A., Department of Physiology, Faculty of Medicine, Izmir Kâtip Çelebi University, Izmir, Turkey; Yigitturk, G., Department of Histology, Faculty of Medicine, Mugla University, Mugla, Turkey; Erbas, O., Department of Physiology, Faculty of Medicine, Bilim University, Istanbul, Turkey; Taskıran, D., Department of Physiology, Faculty of Medicine, Ege University, Izmir, Turkey | en_US |
dc.identifier.pmid | 33874839 | en_US |
dc.identifier.scopus | 2-s2.0-85104732776 | en_US |
dc.authorscopusid | 57189713929 | |
dc.authorscopusid | 56376463500 | |
dc.authorscopusid | 55469991100 | |
dc.authorscopusid | 6603891738 | |