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Neuroprotective effect of phoenix dactylifera (date palm) on paraquat triggered cortico-nigral neurotoxicity
Hope Dike Edobor1, Sunday Abraham Musa2, Uduak Emmanuel Umana1, Gbenga Peter Oderinde3, Abel Nosereme Agbon2
1 Department of Human Anatomy, Faculty of Basic Medical Sciences, College of Medical Sciences, Ahmadu Bello University (ABU); Neuroanatomy and Neurosciences Research Unit, Department of Human Anatomy, ABU, Zaria, Nigeria
2 Department of Human Anatomy, Faculty of Basic Medical Sciences, College of Medical Sciences, Ahmadu Bello University (ABU); Microscopy and Stereology Research Unit, Department of Human Anatomy, ABU; Neuroanatomy and Neurosciences Research Unit, Department of Human Anatomy, ABU, Zaria, Nigeria
3 Department of Human Anatomy, Faculty of Basic Medical Sciences, College of Medical Sciences, Ahmadu Bello University (ABU); Microscopy and Stereology Research Unit, Department of Human Anatomy, ABU, Zaria, Nigeria
Correspondence Address:
Gbenga Peter Oderinde
Department of Human Anatomy, Faculty of Basic Medical Sciences, College of Medical Sciences, Ahmadu Bello University, Zaria, Kaduna
Nigeria
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/jnbs.jnbs_28_21
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Background: Herbicides including paraquat (PQ) have been reported to have deleterious effects on biological systems and normal functioning of the brain, especially regions related to motor functionality and coordination like the cerebrum and substantia nigra resulting in neurodegenerative conditions such as Parkinson's disease. Phoenix dactylifera has high nutritional value and is beneficial in the management and treatment of diverse ailments. Aim: This study assessed the protective properties of Aqueous fruit extract of P. dactylifera (AFPD) on PQ-triggered cortico-nigral neurotoxicity in rats. Neuroprotective properties of AFPD were assessed using beam walking performance (BWP) for motor coordination, oxidative stress biomarkers (Malondialdehyde [MDA], superoxide dismutase [SOD], and glutathione [GSH]) and histological examination (H and E stained) for cytoarchitectural changes. BWP across the study period revealed no motor coordination deficit with PQ exposure. Materials and Methods: Twenty-five rats were categorized into five groups (n = 5); the control was administered 2 ml/kg distilled H2O, another group received 11.35 mg/kg PQ, another received 11.35 mg/kg PQ + 10 mg/kg L-dopa as reference drug, while two other groups received 11.35 mg/kg PQ + 500 mg/kg AFPD and 11.35 mg/kg PQ + 1,000 mg/kg AFPD, respectively, for 28 days. Results: PQ-treated group revealed oxidative stress by significant elevation of MDA levels and decrease in antioxidant enzymes (SOD and GSH). Remarkable cytoarchitectural distortions were observed with PQ treatment. However, AFPD treatment showed ameliorative properties by a significant decrease in MDA levels and increased SOD and GSH activities. Mild distortion-to-relatively normal neuronal cytoarchitecture relative to the control was also observed with AFPD treatment. Conclusion: AFPD possesses potential neuroprotective properties against PQ-triggered pathological changes in cortico-nigral structures of Wistar rats.
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