Morin attenuates trimethyltin-induced hippocampal neurotoxicity in male rats by mitigating oxidative stress, inflammation, and apoptosis

Open Field, Y-maze, Radial Arm Maze (RAM), and Elevated Plus Maze (EPM) tests. Systemic oxidative stress, hippocampal malondialdehyde (MDA), interleukin (IL)-6, and tumor necrosis factor-alpha (TNF-α) were quantified. Histological changes in CA1/CA3 subfields were evaluated using H&E and NeuN/cleaved caspase-3 double immunofluorescence. TMT impaired memory, increased anxiety, and induced oxidative stress, inflammation, and apoptosis. While morin did not alter TMT-induced hyperlocomotion in the open field, the 50 mg/kg dose effectively normalized exploratory activity and significantly attenuated spatial memory impairments in Y-maze and RAM (50 mg/kg). Morin also reduced anxiety-like behavior and suppressed oxidative stress and pro-inflammatory cytokine concentrations. Furthermore, morin preserved neuronal density, reduced non-neuronal hypercellularity, and decreased the apoptotic index in CA1/CA3 subfields. In conclusion, morin exerts robust neuroprotective effects by mitigating inflammation and apoptosis, providing novel evidence for its therapeutic potential against TMT-induced neurodegeneration, with 50 mg/kg identified as the most consistently effective dose.