Histological and histochemical assessements on the effect of ethanol fruit extract of Phoenix dactylifera L. (Date Palm) on cerebral cortex of lead acetate treated wistar rats

Abstract

This study histologically and histochemically assess the effect of ethanol fruit extract of Phoenix dactylifera L. (EFPD) on the cerebral cortex of lead acetate exposed Wistar rats. Twenty rats were grouped into five groups (A to E, n=4). Group A (control) was administered distilled water (2 ml/kg), while groups B to E were treatment groups. Cerebral damage was induced in rats by the administration of lead acetate (120 mg/kg). Groups B, C, D and E were administered lead acetate (120 mg/kg) for a period of 3 weeks, after which groups C and D were administered EFPD (500 and 1000 mg/kg, respectively) and group E was administered dimercaptosuccinic acid (10 mg/kg) for 2 weeks. All administrations were via oral route, once daily. Microscopic examination of cerebral sections of lead acetate-treated rats revealed histo-architectural alteration; cortical degenerative changes, such as, necrosis, satellitosis, vacuolation and neuronal cytoplasmic shrinkage. However, administration of EFPD remarkably ameliorated lead acetate-induced cortical cerebral degenerative changes in the rats, in a dose dependently manner, as compared to the reference drug dimercaptosuccinic acid. Results suggest that EFPD is a potential therapeutic agent against lead acetate-induced cortical cerebral alterations in Wistar rats.

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“…In this study, the histological and histochemical analyses of the cerebral cortex from lead‐induced rats revealed marked cerebral damage with prominent alterations in the neuronal cells and necrosis, which resulted in a significant increase in the number of nonviable cells observed. Findings in this study are in agreements with the work of Sidhu and Nehru ( 2004 ), Mahmoud and Sayed ( 2016 ), and Lazarus et al ( 2018 ), who reported extensive histoarchitectural distortions on the cerebral cortex of mice and rats characterized by cellular shrinkages, vacuolations, neuronal cell damages, hyperchromatic cells, and pyknosis due to lead intoxication. Furthermore, the present study demonstrated multiple pathological lesions on the cerebellum of lead‐induced rats.…”

“…Exposure to metals such as lead has been reported to be one of the leading causes of cerebral and cerebellar toxicity (Sidhu & Nehru, 2004 ). Cerebrum is the largest part of the brain responsible for superior brain functions such as motor movement, emotions, learning, and recognition, while the cerebellum is the major structure of the hindbrain responsible for motor coordination and balance (Lazarus et al, 2018 ; Mahmoud & Sayed, 2016 ). Both cerebellum and cerebrum are delicate structures that are vulnerable to intoxication resulting in a deficit of cognitive abilities and impaired motor coordination and balance (Bhattacharjee et al, 2018 ; Patrick, 2006b ).…”