Microscopic Assessments of the Effect of Phoenix dactylifera L. in a Rat Model of Mercury‑Triggered Cerebral M1 Changes

Abstract

Context: Mercury is a widespread environmental and industrial pollutant that exerts toxic effects on vital organs. The cerebrum, composed of cortical areas such as the primary motor cortex (M1), is a vulnerable target of mercury toxicity within the central nervous system. Phoenix dactylifera is used in folk medicine to treat diverse disorders, such as loss of consciousness, memory disturbances, and nervous disorders. Aim: This study microscopically evaluated the neuroprotective effect of aqueous fruit pulp extract of P. dactylifera (AFPD) on mercury‑triggered M1 changes in Wistar rats. Materials and Methods: Twenty‑four Wistar rats were divided into six groups(I–VI; n = 4). Group I was administered distilled water (2 ml/kg); Group II administered mercuric chloride (MCL, 5 mg/kg); Group III administered Vitamin C (100 mg/kg) + MCL (5 mg/kg); GroupsIV, V, and VI were administered AFPD (250 mg/kg, 500 mg/kg, and 1000 mg/kg, respectively) followed by MCL (5 mg/kg). Neuroprotective property was evaluated by microscopic assessment of M1 region applying histological techniques and analysis of histometric features of M1 neurons. Statistical Analysis Used: One‑way ANOVA and paired sample t‑test were used. Results: Microscopic examination of MCL‑treated cerebral sections revealed M1 histoarchitectural distortion and neurodegenerative changes such as pyknosis, neuronal shrinkage, chromatolysis, loss of pyramidal neurites, and altered Nissl substance reactivity, relative to the control. Administration of AFPD remarkably ameliorated MCL‑triggered M1 changes, especially at dose 500 mg/kg with neuro-protective property comparable to the reference drug, Vitamin C. Conclusion: AFPD is potentially efficacious in ameliorating mercury‑triggered microscopic alterations in M1 region of Wistar rats. The neuroprotective property of AFPD could be attributed to antioxidant properties of constituent phytochemicals.