The protective efficacy of omega-3 polyunsaturated fatty acids on oxidative stress, inflammation, neurotransmitter perturbations, and apoptosis induced by monosodium glutamate in the brain of male rats
Exaggerated neuronal excitation by glutamate is a well-known cause of excitotoxicity, a key factor in numerous neurodegenerative disorders. This study examined the neurotoxic effect of monosodium glutamate (MSG) in the brain cortex of rats and focused on assessing the potential neuroprotective effec...
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Veröffentlicht in: | Metabolic brain disease 2025-01, Vol.40 (1), p.114, Article 114 |
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Sprache: | eng |
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Zusammenfassung: | Exaggerated neuronal excitation by glutamate is a well-known cause of excitotoxicity, a key factor in numerous neurodegenerative disorders. This study examined the neurotoxic effect of monosodium glutamate (MSG) in the brain cortex of rats and focused on assessing the potential neuroprotective effects of omega-3 polyunsaturated fatty acids (ω-3 PUFAs). Four groups of adult male rats (
n
= 10) were assigned as follows; normal control, ω-3 PUFAs (400 mg/kg) alone, MSG (4 mg/g) alone, and MSG plus ω-3 PUFAs (4 mg/g MSG plus 400 mg/kg ω-3 PUFAs). Biochemical analysis, immunohistochemical, and histological examinations were conducted upon completion of the treatment protocol. Results revealed that MSG significantly increased malondialdehyde, nitric oxide, tumor necrosis factor-α, interleukin 1β, acetylcholinesterase, monoamine oxidase, and caspase-3. However, the MSG-treated group showed a decline in reduced glutathione, catalase, superoxide dismutase, dopamine, and serotonin. In addition, MSG caused histopathological changes in the cortical region which support the biochemical and immunohistochemical analysis. Supplementation of ω-3 PUFAs greatly improved the biochemical, immunohistochemical, and histopathological alterations induced by MSG administration in the brain cortex. Together, these findings revealed a neuroprotective effect of ω-3 PUFAs against MSG-induced toxicity in the brain cortex by attenuating oxidative damage, inflammation, neurochemical perturbations, and apoptosis.
Graphical abstract |
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ISSN: | 1573-7365 0885-7490 1573-7365 |
DOI: | 10.1007/s11011-025-01539-4 |