Brain sciences · 2026
Protective Effects of Gallic Acid on Oxidative and Inflammatory Markers in the Hippocampus and Prefrontal Cortex of a Ketamine-Induced Schizophrenia-like Model.
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Arslan Ali Osman, Cetin Ihsan, Yis Ozgur Mehmet, Akcay Sevdenur, Akcay Guven
Аннотация
BACKGROUND: Schizophrenia is a chronic neuropsychiatric disorder characterized by cognitive impairment, behavioral abnormalities, neuroinflammation, and oxidative stress. Increasing evidence suggests that dysregulated inflammatory cytokines and impaired antioxidant defenses contribute to schizophrenia pathophysiology. This study investigated the neuroprotective and anti-inflammatory effects of Gallic Acid (GA) in a ketamine-induced experimental schizophrenia model.
METHODS: Thirty male Balb/C mice were randomly divided into control, ketamine, and ketamine + GA groups. Schizophrenia was induced with ketamine (25 mg/kg/day) for 7 days, while the treatment group additionally received GA (60 mg/kg/day) for another 7 days. Behavioral tests, including open field, novel object recognition, and tail suspension tests, were performed to evaluate locomotor activity, cognition, and depressive-like behavior. Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-18 (IL-18), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), total antioxidant status (TAS), and total oxidant status (TOS) levels were analyzed in hippocampal and prefrontal cortex tissues to assess inflammatory and oxidative stress-related alterations.
RESULTS: Ketamine induced schizophrenia-like behaviors, including hyperlocomotion, memory impairment, and increased immobility. These behavioral alterations were accompanied by significantly elevated TNF-α, IL-1β, IL-18, and TOS levels, alongside reduced SOD, CAT, GSH-Px, and TAS levels in the hippocampus and prefrontal cortex. GA treatment ameliorated behavioral impairments, restored antioxidant enzymes, increased TAS levels, and reduced pro-inflammatory cytokines and TOS in these brain regions.
CONCLUSIONS: GA exerted neuroprotective effects in the ketamine-induced schizophrenia model by reducing oxidative stress, neuroinflammation, and behavioral deficits. These findings suggest that Gallic Acid may serve as a promising therapeutic candidate for schizophrenia through modulation of inflammatory and oxidative stress pathways.
METHODS: Thirty male Balb/C mice were randomly divided into control, ketamine, and ketamine + GA groups. Schizophrenia was induced with ketamine (25 mg/kg/day) for 7 days, while the treatment group additionally received GA (60 mg/kg/day) for another 7 days. Behavioral tests, including open field, novel object recognition, and tail suspension tests, were performed to evaluate locomotor activity, cognition, and depressive-like behavior. Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-18 (IL-18), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), total antioxidant status (TAS), and total oxidant status (TOS) levels were analyzed in hippocampal and prefrontal cortex tissues to assess inflammatory and oxidative stress-related alterations.
RESULTS: Ketamine induced schizophrenia-like behaviors, including hyperlocomotion, memory impairment, and increased immobility. These behavioral alterations were accompanied by significantly elevated TNF-α, IL-1β, IL-18, and TOS levels, alongside reduced SOD, CAT, GSH-Px, and TAS levels in the hippocampus and prefrontal cortex. GA treatment ameliorated behavioral impairments, restored antioxidant enzymes, increased TAS levels, and reduced pro-inflammatory cytokines and TOS in these brain regions.
CONCLUSIONS: GA exerted neuroprotective effects in the ketamine-induced schizophrenia model by reducing oxidative stress, neuroinflammation, and behavioral deficits. These findings suggest that Gallic Acid may serve as a promising therapeutic candidate for schizophrenia through modulation of inflammatory and oxidative stress pathways.