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Neuroprotective Effects of Phoenix dactylifera L. and Melatonin on Aluminum Chloride-induced Neurotoxicity in the Cerebellum of Adult Male Wistar Rats

Elvis T Godam , Wilson Francisca Cheyachi , Mesole Samuel Bolaji , Musa Abraham Sunday

Neuroprotective Effects of Phoenix dactylifera L. and Melatonin on Aluminum Chloride-induced Neurotoxicity in the Cerebellum of Adult Male Wistar Rats

Exposure to aluminium is associated with neurotoxicity, affecting various parts of the nervous system. The study investigated the neuroprotective potential of ethanolic fruit extract of Phoenix dactylifera (EFPD) and melatonin against aluminium chloride (AlCl3)-induced neurotoxicity in male adult Wistar rats. Rats were divided into six groups: group 1 received 0.2 ml distilled water; group 2 received 5 mg/kg AlCl3; group 3 received 10 mg/kg melatonin and 5 mg/kg AlCl3; group 4 received 500 mg/kg EFPD and 5 mg/kg AlCl3; group 5 received 1000 mg/kg EFPD and 5 mg/kg AlCl3; group 6 received 670 mg/kg vitamin E and 5 mg/kg AlCl3. Extracts were administered for two weeks. At the end of the study, the cerebellum was dissected for histopathological analysis, and blood samples were collected for biochemical assays. Sensory-motor and motor coordination were assessed using Foregrip strength and beam walking tests. Results revealed that oral administration of AlCl3 significantly (p<0.05) increased lipid peroxidation levels (malondialdehyde) and significantly (p<0.05) reduced antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase), leading to neuronal degeneration of Purkinje cells in the cerebellum. However, oral administration of melatonin, EFPD, and vitamin E significantly (p<0.05) decreased lipid peroxidation levels and significantly (p<0.05) increased antioxidant activities, preserving Purkinje cell cytoarchitecture. These findings suggest that Phoenix dactylifera fruit extract and melatonin possess neuroprotective properties against aluminium-induced neurotoxicity, as evidenced by restored antioxidant levels and preserved cerebellar cytoarchitecture. These results highlight the therapeutic potential of natural compounds in mitigating the harmful effects of aluminium toxicity on the central Nervous system.

Key Words: Phoenix dactylifera, Vitamin E, Purkinje cells, antioxidant, aluminium chloride

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