Promising neuroprotective potential of naringenin against trimethyltin-induced cognitive deficits and hippocampal neurodegeneration in rats

Naringenin exhibited a dose-dependent inhibition of CA1 neuronal loss and reversed TMT-induced cognitive deficits. It markedly decreased hippocampal levels of malondialdehyde (MDA), nitrite, tumor necrosis factor-alpha (TNFα), and AChE activity while enhancing catalase and superoxide dismutase (SOD) activities, 3-nitrotyrosine (3-NT) immunoreactivity, and MMP. Furthermore, findings demonstrated that naringenin mitigated the TMT-induced elevation in hippocampal levels of AD-specific proteins, including phosphorylated tau (p-tau), amyloid-beta (Aβ), and presenilin 1. Naringenin may be postulated as a promising therapeutic candidate for AD and related neurodegenerative conditions by mitigating oxidative and nitrosative stress, maintaining mitochondrial integrity, decreasing inflammation, and modulating pathways of neurodegeneration.