{"title":"Lutein Exerts Antioxidant and Neuroprotective Role on Schizophrenia-Like Behaviours in Mice.","authors":"Helia Aziziha, Shahin Hassanpour, Morteza Zendehdel","doi":"10.1002/jdn.10407","DOIUrl":null,"url":null,"abstract":"<p><p>Schizophrenia is an esteemed neuropsychiatric condition delineated by the manifestation which role of the N-methyl-D-aspartate receptor (NMDAR) is important. Lutein administration exhibits protective effects via NMDA receptors. Thus, the main goal of this research was to investigate how lutein can possibly act as an antioxidant and provide protection for the brain against schizophrenia-like behaviours in mice. In total, 24 male mice were divided into four experimental groups: control, ketamine (20 mg/kg, i.p), lutein (10 mg/kg, i.p) and a mix of ketamine (20 mg/kg, i.p) and lutein (10 mg/kg, i.p). Lutein was given to the mice for 30 days, while ketamine was given from Days 16 to 30 to create a model of schizophrenia in the animals. After giving drugs, schizophrenia-like behaviours were evaluated with novel object recognition test (NORT), tail suspension test (TST), forced swimming test (FST) and open field tests. Furthermore, the amounts of brain malondialdehyde (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) were assessed. The findings showed a noteworthy decrease in the crossings during the open field test and increase in immobility duration in the TST and FST as a result of ketamine administration (p < 0.05). Prior administration of lutein showed a decrease in the detrimental effects of ketamine on the open field assay, along with a reduction in immobility duration in the TST and FST experiments (p < 0.05). Administration of ketamine caused a notable reduction in the discrimination index, while pretreatment with lutein was associated with a rise in the discrimination index (p < 0.05). Furthermore, the administration of ketamine significantly increased the levels of MDA in both cortical and subcortical regions, which were then reduced by lutein pretreatment (p < 0.05). Moreover, ketamine use led to a significant decrease in tissue SOD, GPx and CAT levels in both cortical and subcortical brain regions in mice (p < 0.05). Nonetheless, lutein pretreatment significantly enhanced SOD, GPx and CAT levels in cortical and subcortical regions (p < 0.05). These results indicate that lutein may have protective effects on the brain to improve behavioural problems.</p>","PeriodicalId":13914,"journal":{"name":"International Journal of Developmental Neuroscience","volume":"85 1","pages":"e10407"},"PeriodicalIF":1.7000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Developmental Neuroscience","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1002/jdn.10407","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"DEVELOPMENTAL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Schizophrenia is an esteemed neuropsychiatric condition delineated by the manifestation which role of the N-methyl-D-aspartate receptor (NMDAR) is important. Lutein administration exhibits protective effects via NMDA receptors. Thus, the main goal of this research was to investigate how lutein can possibly act as an antioxidant and provide protection for the brain against schizophrenia-like behaviours in mice. In total, 24 male mice were divided into four experimental groups: control, ketamine (20 mg/kg, i.p), lutein (10 mg/kg, i.p) and a mix of ketamine (20 mg/kg, i.p) and lutein (10 mg/kg, i.p). Lutein was given to the mice for 30 days, while ketamine was given from Days 16 to 30 to create a model of schizophrenia in the animals. After giving drugs, schizophrenia-like behaviours were evaluated with novel object recognition test (NORT), tail suspension test (TST), forced swimming test (FST) and open field tests. Furthermore, the amounts of brain malondialdehyde (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) were assessed. The findings showed a noteworthy decrease in the crossings during the open field test and increase in immobility duration in the TST and FST as a result of ketamine administration (p < 0.05). Prior administration of lutein showed a decrease in the detrimental effects of ketamine on the open field assay, along with a reduction in immobility duration in the TST and FST experiments (p < 0.05). Administration of ketamine caused a notable reduction in the discrimination index, while pretreatment with lutein was associated with a rise in the discrimination index (p < 0.05). Furthermore, the administration of ketamine significantly increased the levels of MDA in both cortical and subcortical regions, which were then reduced by lutein pretreatment (p < 0.05). Moreover, ketamine use led to a significant decrease in tissue SOD, GPx and CAT levels in both cortical and subcortical brain regions in mice (p < 0.05). Nonetheless, lutein pretreatment significantly enhanced SOD, GPx and CAT levels in cortical and subcortical regions (p < 0.05). These results indicate that lutein may have protective effects on the brain to improve behavioural problems.
期刊介绍:
International Journal of Developmental Neuroscience publishes original research articles and critical review papers on all fundamental and clinical aspects of nervous system development, renewal and regeneration, as well as on the effects of genetic and environmental perturbations of brain development and homeostasis leading to neurodevelopmental disorders and neurological conditions. Studies describing the involvement of stem cells in nervous system maintenance and disease (including brain tumours), stem cell-based approaches for the investigation of neurodegenerative diseases, roles of neuroinflammation in development and disease, and neuroevolution are also encouraged. Investigations using molecular, cellular, physiological, genetic and epigenetic approaches in model systems ranging from simple invertebrates to human iPSC-based 2D and 3D models are encouraged, as are studies using experimental models that provide behavioural or evolutionary insights. The journal also publishes Special Issues dealing with topics at the cutting edge of research edited by Guest Editors appointed by the Editor in Chief. A major aim of the journal is to facilitate the transfer of fundamental studies of nervous system development, maintenance, and disease to clinical applications. The journal thus intends to disseminate valuable information for both biologists and physicians. International Journal of Developmental Neuroscience is owned and supported by The International Society for Developmental Neuroscience (ISDN), an organization of scientists interested in advancing developmental neuroscience research in the broadest sense.