KOLAVIRON AMELIORATES COGNITIVE DEFICITS AND NEURONAL DEGENERATION INDUCED-BY D-GALACTOSE IN MICE MODEL

 

Olufunto Omodele, ADELEYE^1,2,Munirat Oyindamola, ADEWALE^1,2

¹Department of Anatomy, Ladoke Akintola University of Technology, Ogbomosho, Nigeria

²Eagles’ Research Laboratory, Ladoke Akintola University of Technology, Ogbomosho, Oyo State, Nigeria

*Corresponding Author: Olufunto Omodele Adeleye, (Email: ooadeleye@lautech.edu.ng, ORCID ID: 0000-0003-1398-9180)

ABSTRACT

Background: D-galactose, a naturally occurring monosaccharide, is widely used in experimental models to induce aging. Prolonged exposure to D-galactose has been associated with oxidative stress, mitochondrial dysfunction, neuronal loss, and cognitive decline hallmarks of neurodegenerative diseases such as Alzheimer’s disease. Kolaviron, a biflavonoid complex extracted from Garcinia kola, possesses documented antioxidant and anti-inflammatory properties that may offer neuroprotection. This study investigates the neuroprotective potential of kolaviron against D-galactose-induced hippocampal toxicity in mice.

Aim: To evaluate the efficacy of kolaviron in mitigating D-galactose-induced cognitive deficits, oxidative stress, neuroinflammation, and histopathological damage in the hippocampus.

Method: Thirty-six adult albino mice (20–22 g) were assigned to six groups including control, D-galactose (50 mg/kg), kolaviron (400 mg/kg), and co-treatment groups. Neurobehavioral tests Open Field Test, Y-Maze, and Novel Object Recognition assessed anxiety, locomotor activity, and memory. Biochemical assays measured oxidative stress markers (MDA, GSH, SOD, catalase), inflammatory cytokines (TNF-α, IL-6), and acetylcholinesterase activity. Hippocampal histology was evaluated via H&E staining. Data were analyzed using ANOVA with significance at p ≤ 0.05.

Results: D-galactose exposure significantly impaired memory and locomotion, increased anxiety, elevated MDA and nitrite levels, and reduced antioxidant enzyme activity and AChE function. It also caused hippocampal pyramidal cell degeneration. Kolaviron, particularly in post-treatment, reversed these effects by improving behavioral performance, restoring antioxidant and anti-inflammatory balance, and ameliorating histological damage.

Conclusion: Kolaviron confers significant neuroprotection against D-galactose-induced hippocampal toxicity, likely through antioxidative and anti-inflammatory pathways. These findings suggest its therapeutic potential for neurodegenerative disorders such as Alzheimer’s disease.

Keywords: Kolaviron, D-galactose, Neuroprotection, Oxidative stress, Inflammation, Cognitive impairment, Hippocampus