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.

This study was to evaluate the effects of aqueous and ethanol fruit extracts of Phoenix dactylifera on the cerebellar cortex of Artesunate-Amodiaquine (AS-AQ) treated Wistar rats. Thirty-six adult male Wistar rats were randomly divided into nine groups (n=4). Group 1 served as the control; Group 2 received 2.86/8.75 mg/kg AS-AQ. Group 3 received 2.86/8.75 mg/kg AS-AQ + 100 mg/kg ascorbic acid; Groups 4, 5 and 6 received 2.86/8.75 mg/kg AS-AQ + 500 mg/kg aqueous extract of P. dactylifera (AEPD), 2.86/8.75 mg/kg AS-AQ + 1000 mg/kg AEPD and 2.86/8.75 mg/kg AS-AQ + 1500 mg/kg AEPD respectively. Groups 7, 8 and 9 received 2.86/8.75 mg/kg AS-AQ + 500 mg/kg ethanolic extract of P. dactylifera (EEPD), 2.86/8.75 mg/kg AS-AQ + 1000 mg/kg EEPD and 2.86/8.75 mg/kg AS-AQ + 1500 mg/kg EEPD respectively. All administration was orally done, and lasted for 28 days. Evidences of necrosis, chromatolysis and vacuolations were observed in the cerebellar cortex of the AS-AQ treated group. The histoarchitecture of the AEPD and EEPD treatment groups were preserved in a dosedependent manner, and compared positively to the reference drug ascorbic acid treatment, with the AEPD-treated groups being better preserved. Amelioration of the severity of neurodegeneration by the extracts suggest that the extracts could have exerted their ameliorative effects by antioxidant activities ascribed to the phytochemicals present in the extracts.