Lutein Exerts Antioxidant and Neuroprotective Role on Schizophrenia-Like Behaviours in Mice.

Lutein, an antioxidant, may protect the brain against schizophrenia-like behaviors in mice. In a study with 24 male mice, ketamine was used to induce schizophrenia-like symptoms. Mice pretreated with lutein for 30 days before and during ketamine exposure showed fewer behavioral deficits: they moved more in open field tests and spent less time immobile in tail suspension and forced swimming tests, indicating reduced depression-like behavior. Lutein also improved object recognition memory. At the brain chemistry level, ketamine increased malondialdehyde (a marker of oxidative stress) and decreased antioxidant enzymes superoxide dismutase, glutathione peroxidase, and catalase in cortical and subcortical regions. Lutein pretreatment reversed these changes, raising antioxidant levels and lowering oxidative stress. The findings suggest lutein may help improve behavioral problems linked to schizophrenia.

Study at a glance

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.