Chloroform fruit extract of Phoenix dactylifera L. (Date Palm) has neuroprotective effect against lead acetate-induced neurotoxicity in Wistar rats
DOI:
https://doi.org/10.4314/jeca.v22i1.1Keywords:
Phoenix dactylifera L, Cerebrum, Cerebellum, Histology, Oxidative stress, Wistar ratsAbstract
Background and aim: Environmental and health hazards posed by lead, a heavy metal contaminant, in water and other media are rising. Different solvent-extract forms of the Phoenix dactylifera plant are of vast medicinal benefits. The neuroprotective effect of chloroform fruit pulp extract of P. dactylifera (CFPD) was assessed on lead acetate-induced cerebellar and cerebral toxicity in Wistar rats.
Materials and methods: Twenty-four rats were divided into six groups: (A – F; n= 4): the control (group A) was administered distilled water (2 ml/kg p.o); group B received lead acetate (LA, 120 mg/kg body weight p.o) only; group C, received vitamin C (100 mg/kg body weight p.o) as reference drug concomitantly followed by LA (120 mg/kg body weight p.o); groups (D, E, F) received CFPD (125 mg/kg body weight, 250 mg/kg body weight and 500 mg/kg body weight p.o, respectively) concomitantly followed by LA (120 mg/kg body weight). Administrations lasted for 14 days. The neuroprotective effect of CFPD was evaluated using histological (H&E) stained sections of cortical cerebellar and cerebral– (layers III and V) regions as well as biochemical (oxidative stress markers; serum malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase) assessments.
Results: Results revealed neurodegenerative changes in the LA-treated group's cerebellar and cerebral cortices, including perineuronal vacuolation and gliosis. However, the administration of CFPD remarkably ameliorated LA-induced cerebellar and cerebral changes. Relative to the control, the LA-treated group showed altered serum oxidative stress markers, which were ameliorated (p<0.05) with CFPD treatment.
Conclusion: Results suggest that CFPD, especially at a dose of 250 mg/kg, has neuroprotective potential against LA-induced cerebellar and cerebral toxicity in rats which could be attributed to antioxidant properties.
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