Thymol mitigates monosodium glutamate-induced neurotoxic cerebral and hippocampal injury in rats via overexpression of nuclear erythroid 2-related factor 2 signaling pathway as well as altering nuclear factor- kappa β and glial fibrillary acidic protein expression

Résumé

Abstract Monosodium glutamate (MSG) is commonly used in various food industries as a flavor enhancer. MSG is reported to cause many toxic effects, including increased neurotoxicity. The study investigates the molecular mechanisms underlying thymol's neuroprotective effect against MSG-induced neurotoxic cerebral and hippocampal injury in rats. Brain injury was induced by MSG (2 g/kg; i.p.) for 15 days. Thymol (400 & 800 mg/kg/day; p.o.) was administered along with MSG. MSG control rats showed a significant reduction in behavioral activity, elevated brain tissue oxidative stress, inflammatory parameters, Nrf2 gene up-regulation, overexpression of nuclear factor-kappa β (NF-kβ), glial fibrillary acidic protein (GFAP) as well as neuronal damage in the cerebral cortex & hippocampus. Thymol ameliorated MSG-induced brain injury via overexpression of the Nrf2 gene, thus increasing the cellular defense and organizing antioxidant & anti-inflammatory effects. Thymol improved behavioral activity and brain tissue GSH content. Thymol also decreased brain contents of MDA, NO, TNF-α & IL-6. Moreover, Thymol improved NF-kβ & GFAP immunohistochemical expression and histopathological picture in the cerebral cortex & hippocampus compared to MSG control rats. The aforementioned results suggest that thymol exhibits promising neuroprotective effects. The study elucidates the molecular mechanisms linking Nrf2 pathway signaling to oxidative stress, inflammation & NF-kβ expression underlying thymol’s protection against MSG-induced neurotoxicity. The study also highlights the role of GFAP expression in MSG-induced astrocyte injury of cerebrum & hippocampus of rats and the promising protective effects of thymol in ameliorating astrocyte injury.

Citer ce document

Accès au document

Ce document est hébergé sur son dépôt institutionnel d'origine.

Auteur(s)

Statistiques

Consultations : 1

Téléchargements : 0