Omega-3 fatty acid reverses Ketamine-induced hyperlocomotion, memory deficit and cerebral cortex neuronal injury in rats
Acta Bioscientia: Journal of Biomedical and Biological Science Research January 25, 2025 DOI: 10.71181/actabioscientia12170 (opens in new tab) via Semantic Scholar
Summary
AI-generated from the abstractOmega-3 fatty acids (OMG) may protect against brain changes caused by ketamine in rats. Rats given ketamine showed increased movement, memory impairment, and higher oxidative stress and inflammation. Treatment with OMG at 250 or 500 mg/kg reversed these effects, similar to the antipsychotic olanzapine. Ketamine also caused neuronal degeneration in the cerebral cortex, which OMG partially reversed. The findings suggest OMG has neuroprotective potential, but more research is needed to confirm benefits in humans.
Study at a glance
| Characteristics | Randomized controlled trial Peer reviewed |
|---|---|
| Sample size | 50 |
| Population | Rats (130-150g) |
| Interventions | Omega-3 fatty acids Olanzapine |
| Dose | 250 and 500 mg/kg orally for omega-3 fatty acids; 2 mg/kg for olanzapine |
| Duration | 14-day treatment period |
| Keywords | Medicine |
| Key finding | Omega-3 fatty acids reversed ketamine-induced behavioral changes, oxidative stress, inflammation, and neuronal degeneration in rats. |
Abstract
Schizophrenia (SZ) a chronic debilitating mental disorder affecting approximately 1% of the population globally. While understanding of pathophysiology, neuropathology and treatment have advance significantly; resistance to therapy and treatment failures necessitate the search for novel compounds like omega-3 fatty acids (OMG). This study investigated the effects of OMG on ketamine-induced brain changes in rats. Fifty rats (130-150g) were assigned into five groups (n=10); group A (control) received distilled water intraperitoneally (i.p.), while rats in groups B-E were treated with ketamine (15 mg/kg i.p) for 10 days. Subsequently, rats in groups A and B (Ketamine control) received distilled water orally at 10 ml/kg while C and D received OMG at 250 and 500 mg/kg orally. Rats in group E received olanzapine (standard therapy) at 2 mg/kg, Treatments were for 14 days following which animals were exposed to the open field arena, elevated Plus and Y-Maze. Twenty-four hours after the last test rats were euthanised, and blood was taken for estimation of malondialdehyde (MDA), Total antioxidant capacity (TAC), and interleukin (IL)-6 and -1β. The cerebral cortex was sectioned and processed for histological analysis. Results showed an increase in horizontal locomotion and rearing, memory impairment and increased oxidative stress and proinflammation with ketamine, which was reversed with OMG at 250 and 500 and olanzapine . Cerebral cortex histomorphology revealed presence og neuronal degeneration with ketamine and variable degrees of reversal with OMG and Olanzapine. In conclusion this study demonstrated the possible neuroprotective effects of OMG in mitigating ketamine induced changes in rats. However, more studies would be required to ascertain its benefits in humans