Flavonoid naringin inhibits microglial activation and exerts neuroprotection against deltamethrin induced neurotoxicity through Nrf2/ARE signaling in the cortex and hippocampus of rats
Microglial activation and oxidative stress contribute in the pathogenesis of neurotoxicity elicited by toxicant. This study was conducted to evaluate the potential neuro protective role of naringin on deltamethrin (DLM) induced neurotoxicity in rats. DLM-induced neuronal oxidative stress was evidenced by significantly increased level of lipid peroxidation and significantly reduced levels of antioxidant enzymes were observed in DLM-induced rats. DLM-induced neuronal damage was also evidenced by TEM analysis and histopathological amendments of DLM administered rat brain by H & E and Cresyl violet staining. DLM-induced microglial mediated neurotoxicity was proven by a significant overexpression of GFAP in DLM-induced rats. Thus, it is proposed that the DLM exerts its neurotoxic effects possibly via the mechanism of microgliosis and oxidative stress. In this present study naringin supplementation promoted the Nrf2 dissociation of Keap-1 and its nuclear translocation in the brain is likely to contribute to neuro protective effects of naringin evidenced by up-regulation of antioxidant enzymes, and attenuation of lipidperoxides formation. Naringin supplementation also controls the abnormalities of DLM-induced microglial activation by significantly attenuates the GFAP expression. Altogether, our data clearly indicate that an activation of Nrf2/ARE pathways in brain by naringin protects brain from DLM-induced neurotoxicity.
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