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ABSTRACT
Neurological disorders can cause cognitive and memory impairments, often triggered by neurotoxic heavy metals like nickel chloride. Nickel infiltrates the brain by crossing the bloodbrain barrier, where it generates oxidative stress, resulting in hippocampal damage and subsequent impairments in learning and memory. Antioxidants like quercetin have shown potential in protecting the hippocampus from oxidative damage, offering a possible solution to nickel-induced neurotoxicity. Accordingly, the aim of this study was to assess the neurobehavioral activity of quercetin on nickel chloride-induced hippocampal toxicity in adult Wistar rats. Forty-eight (48) Wistar rats were randomly divided into six (6) groups of eight (8) rats each: Group A (Control) received 1 mL of sterile water. Group B received 5 mg/kg body weight of Nickel Chloride only. Group C received 50 mg/kg body weight of Quercetin and 5 mg/kg body weight of Nickel Chloride. Group D received 100 mg/kg body weight of Quercetin and 5 mg/kg body weight of Nickel Chloride. Group E received 50 mg/kg body weight of Quercetin only. Group F received 100 mg/kg body weight of Quercetin only. Administration lasted for 28 days after which neurobehavioral assessment was carried out using the elevated plus maze test, antioxidant enzymes activity and lipid peroxidation concentration was assessed as well as the histology of the hippocampus. Insilico assessment for quercetin against Ache and amyloid-beta was also carried out. Findings from this study revealed that nickel-exposed rats demonstrated weight loss and increased transfer latency, decreased antioxidant enzymes activity, increased malondialdehyde concentration, as well as atrophied and vacuolated pyramidal cells and astrocytes in the hippocampus. However, pre-treatment with quercetin enhanced body weight, reduced neurobehavioral deficits by shortening transfer latency, boosted antioxidant enzyme activity, lowered lipid peroxidation levels, and alleviated histological changes in the hippocampus, as evidenced by a largely preserved hippocampal structure. Furthermore, quercetin demonstrated strong binding affinities against AChE and Amyloid-beta similar to Donepezil. In conclusion, findings from this study suggest that quercetin possesses neuroprotective properties against nickel chloride-induced hippocampal deficits in Wistar rats.
