Ameliorative Effects of Kolaviron on Behavioural Deficits and Oxidative Damage in Prefrontal Cortex and Hippocampus of Cuprizone-Induced Demyelinated Mice

Abstract

Cuprizone neurotoxicity is commonly induced to mimic demyelinating disorders of the central nervous system, especially multiple sclerosis. This study assessed the role of kolaviron, a Garcinia kola biflavonoid, in restoring behavioural functions in cuprizone-induced neurotoxicity after termination of cuprizone treatment. Eighteen adult male Swiss albino mice aged between 6-8 weeks were randomly divided into 3 equal groups (A to C). Group A (control) mice were fed with normal rodent diet while groups B and C received 0.2% cuprizone diet for 5 weeks to induce demyelination; thereafter group B mice with cuprizone-induced demyelination were administered corn oil (0.5 mL), while group C mice with cuprizone-induced demyelination were administered kolaviron (200 mg/kg/d) for 14 days. The mice were assessed for learning, memory, anxiety and exploratory drive, and thereafter the concentration of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in the prefrontal cortex and hippocampus of the mice were evaluated. Findings revealed improved behavioural outcomes in mice treated with kolaviron compared to control and the untreated cuprizone-induced demyelinated mice. There was significant reduction in SOD and GPx activities with significant increase in MDA concentration in the untreated cuprizone-induced mice compared to controls. However, there was significant increase in SOD and GPx activities with significant reduction in MDA concentration in the kolaviron-treated cuprizone-induced mice compared to those of untreated cuprizone-induced mice. The results suggest that kolaviron may effectively ameliorate the oxidative damage and behavioural deficits associated with cuprizone-induced neurotoxicity.