Abstract
Aim: This study was to histologically assess the therapeutic effect of aqueous fruit extract of Phoenix dactylifera (AFEPD) on lead acetate-induced cerebellar damage in Wistar rats. Methods: Twenty four rats were grouped into six (I–VI; n=4). Group I (control) received distilled water (1 ml/kg). Group II received lead acetate (LA, 120mg/kg) only. Groups III and IV received LA (120mg/kg) followed by AFEPD (1000mg/kg and 1500mg/kg, respectively). Groups V and VI received AFEPD (1000mg/kg and 1500mg/kg, respectively). All administrations were by oral route. Treatment lasted 28 days; LA was administered from day 1 to day 14, while AFEPD was administered from day 15 to day 28 of the experimental period. Therapeutic activity of AFEPD was assessed by histological examination of the cerebellar cortex with H and E stain. Results: Findings revealed neurodegenerative changes in the cerebellar cortex like perineuronal vacoulations and cytoplasmic shrinkage in molecular layer cells and Purkinje cells in LA-intoxicated group. The administration of AFEPD remarkably ameliorated LA–induced cerebellar damage dose dependently. Normal cerebellar histoarchitecture was observed with administration of AFEPD only. Conclusion: Results suggest that AFEPD has therapeutic potentials against lead acetate-induced cerebellar damage in Wistar rats. Key words: Cerebellum, Lead acetate, Phoenix dactylifera
Highlights
Lead poisoning is a well-known public health risk especially in developing countries (Flora et al, 2012)
The aim of this study was to histologicallyassess the therapeutic effect of aqueous fruit extract of Phoenix dactylifera (AFEPD) on lead acetateinduced cerebellar damage in Wistar rats
All administrations were by oral route and the treatment lasted for twenty-eight days; lead acetate (LA) was administered from day 1 to day 14, while AFEPD was administered from day 15 to day 28 of the experimental period
Summary
Lead poisoning is a well-known public health risk especially in developing countries (Flora et al, 2012). Lead is highly toxic and can interrupt the body’s neurological, biological and cognitive functions (Elombah and HRW, 2012; Bauchi et al, 2016). The involvement of the nervous system in lead toxicity is well known (Martin et al, 1970; ElNeweshy and El-Sayed, 2011). Cerebellar dysfunction may occur in association with exposure to a wide variety of toxins including heavy metals (such as mercury, lead, thallium, and manganese), drugs and solvents. These toxins may adversely affect the cerebellum directly or as part of a more generalized encephalopathy (Fredericks, 2011)
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