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article · NIgerian Journal of Neuroscience

Spondias mombin L. Fruit Pulp Prevents D-Galactose-Induced Cognitive Deficits, Oxidative Stress and Neurodegeneration in Wistar Rats' Prefrontal Cortex

2025Open accessOsun State University

Abstract

D-galactose (D-Gal) administration is known to cause cognitive impairment in animal models of ageing. Spondias mombin L. fruit pulp (SM) is known to ameliorate stress-induced conditions caused by oxidative stress. The neuroprotective role of SM against D-Gal-induced stress in Wistar rats was investigated. Forty-two male Wistar rats were divided into six groups (n=7): control group were fed with normal diet; D-Gal group were treated with D-Gal only; Gal + SM5 group were fed with 5% SM (w/w)-containing diet and treated with D-Gal; Gal + SM10 group were fed with 10% SM (w/w)-containing diet and treated with D-Gal; SM 5 group were fed with 5% SM-containing diet; and SM 10 group were fed with 10% SM-containing diet. Control, SM5, and SM10 groups were treated by 0.9% sodium chloride/day (subcutaneous (s.c), 5 days per week) while D-Gal treatment was 250 mg/kg of D-Gal (s.c., 5 days per week). Administration was done for 6 weeks after which behavioural assessments were conducted, followed by biochemical and histopathological analyses of the prefrontal cortex. The administration of SM-containing diet at the two concentrations investigated in this study showed improvements in cognitive impairment caused by the D-Gal compared to the control. Biochemical assays indicated that D-Gal significantly disrupted antioxidant status, proinflammatory and anti-inflammatory cytokines. SM supplementation reversed these effects. Histopathological analysis confirmed that SM5 and SM10 significantly reversed D-Gal-induced cortical alterations. In conclusion, SM attenuated D-Gal-induced cognitive deficits, oxidative stress, and neurodegeneration in Wistar rats.

Research topics

  • Antioxidants, Aging, Portulaca oleracea
  • Diet, Metabolism, and Disease
  • GABA and Rice Research

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DOI: 10.47081/njn2025.16.2/002

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