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Neuroprotective Effect of Jobelyn® on Ketamine-Induced Schizophrenia-Like Behaviors and Oxidative Damage in Mice Brain

Itivere Adrian Omogbiya, Benneth Ben‐azu, Maxwell Oboh, Oruese Orovwigho, Tarela M E Daubry, Solomon Umukoro

Pharmacology and Toxicology of Natural Medicines July 7, 2026 Peer reviewed DOI: 10.52406/ptnm.v6i4.176 via OpenAlex

Summary

Jobelyn® (JB) demonstrated the ability to prevent and reverse schizophrenia-like behaviors and oxidative damage induced by ketamine in mice. The study showed that JB significantly countered ketamine-induced hyperlocomotion and memory impairment, as well as improved levels of oxidative stress markers such as superoxide dismutase, catalase, and glutathione, while reducing thiobarbituric acid-reactive substances. These findings support the potential of JB as a novel antipsychotic agent with neuroprotective antioxidant properties.

Study at a glance

Design experimental study
Population mice
Key finding Jobelyn® effectively prevented and reversed schizophrenia-like behaviors and oxidative alterations induced by ketamine.

Abstract

Background and Purpose: Schizophrenia is a chronic, debilitating psychiatric disorder affecting many young adult populations worldwide. Evidence from studies of central changes in the oxidative defense system suggests the involvement of oxidative stress in the pathophysiology of schizophrenia. Jobelyn® (JB) is a commercial polyherbal formulation that has been documented to show beneficial effects on psychosis. Preliminary evidence from animal studies suggests that JB is efficacious in animal models of schizophrenia. This study investigated the effects of JB in the prevention and reversal of ketamine-induced schizophrenia-like behaviors and oxidative damage in mice. Methods: In the reversal protocol, mice received ketamine (20 mg/kg, i.p.) or saline for 14 days, and JB (5, 10, or 50 mg/kg), risperidone (0.5 mg/kg, i.p.), or vehicle from days 8 to 14. In the prevention protocol, mice were pretreated with JB (5, 10, or 50 mg/kg daily), risperidone, or vehicle prior to ketamine. Behaviors related to positive (locomotor activity) and cognitive (Y-maze test) symptoms of schizophrenia were also assessed. Oxidative stress markers, including superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and thiobarbituric acid-reactive substances (TBARS) levels, were measured in the whole brain. Results: JB and risperidone significantly (P<0.05) prevented and reversed ketamine-induced hyperlocomotion and memory impairment. Ketamine-induced reductions (P<0.05) in SOD, CAT, and GSH levels, alongside increased TBARS content, were ameliorated by JB (P<0.05). These data provide a rationale for evaluating JB as a novel antipsychotic agent and suggest that its mechanism of action includes a neuroprotective antioxidant mechanism. Conclusion: Our findings showed that Jobelyn® prevented and reversed schizophrenia-like behavioral and oxidative alterations induced by ketamine.

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