Neurobehavioral, and Cytoarchitecture Evaluation of the Therapeutic Potential of n‐butanol fraction of Phoenix dactylifera L. on lead acetate triggered neurodegenerative changes in Wistar rats

Abstract Background Lead, a pervasive and toxic environmental pollutant, of particular concern is its impact as a trigger for neurodegenerative diseases. Phoenix dactylifera (date palm), has garnered attention due to its pharmacological properties: antioxidant and anti‐inflammatory, attributed to its rich flavonoid content. This assessed the therapeutic potentials of n‐ butanol fraction of P. dactylifera (BFPD) on the behavioral and histomorphology of hippocampus lead acetate (PbA)‐induced neurotoxicity in Wistar rats. Method Forty‐two rats were categorized into seven groups ( n = 7). Two experimental phases were employed: Toxicity‐phase, and Treatment‐phase. Toxicity‐phase: all rats received PbA (120 mg/kg), for 14 days, except group one (control); Treatment‐phase: group II (sacrificed), group III (Natural recovery), while groups (IV‐VII) received (500 mg/kg, 750 mg/kg and 1000 mg/kg) n‐ BFPD and (100 mg/kg) vitamin C (as reference antioxidant). Treatment was via oral route, which lasted for 28 days. Therapeutic properties of n‐ BFPD were assessed using Neurobehavioral assessment: Morris water maze performance and Novel object recognition test for (spatial memory, learning, and cognition); Oxidative stress biomarkers were assay using Malondialdehyde [MDA], and Superoxide dismutase [SOD], and microscopic hippocampus examination (CA1 and CA3) using histological and histochemical staining techniques and quantification of Nissl substance stain intensity using a computer running image analysis software (imageJ). Result PbA‐treated group revealed neurodegenerative changes as remarkable ( p<0.05) memory, learning and cognition impairment, elevation MDA levels and decrease in antioxidant enzymes (SOD), and cytoarchitectural distortions evidenced by necrotic nuclei, vacuolation and pyknosis, compared to the control. However, treatment with n‐ BFPD revealed cognitive improvement in memory and learning; decreased MDA levels and increased SOD activities. Mild distortion‐to‐relatively normal neuronal cytoarchitecture relative to the control was also observed with n‐ BFPD treatment. Conclusion n‐ BFPD possesses potential therapeutic properties against PbA‐induced neurobehavioural and cognitive deficit and pathological changes which are indicator of neurodegenerative diseases. Keyword : cytoarchitecture, cognition, neurodegeneration