Browsing by Author "Gbadamosi I.T."

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    Moringa oleifera ameliorates cuprizone-induced cerebellar damage in adult female rats
    (College of Health Sciences, Osun State University, 2018) Omotoso G.O.; Kadir R.E.; Lewu S.F.; Gbadamosi I.T.; Akinlolu A.A.; Adunmo G.O.; Kolo R.M.; Lawal M.O.; Ameen M.O.
    Objectives: Cuprizone is a neurotoxicant used in modeling demyelinating disorders. This study explored the effects of Moringa oleifera (MO) on oxidative, histomorphological and behavioural changes in cuprizone-damaged cerebellum. Methods: Twenty adult female Wistar rats were grouped into 4, each group having five animals. Group A received 1 ml of normal saline (Control); group B received 0.4% cuprizone; group C received 15.6 mg/kgBW Moringa oleifera leaf extract; group D received 0.4% cuprizone and 15.6 mg/kgBW Moringa oleifera, orally for 5 weeks. The animals were assessed for exploratory and locomotor activities, while the cerebellum was processed for histology and assayed for nitric oxide (NO), catalase (CAT) and superoxide dismutase (SOD) activities. Results: Cuprizone treatment caused weight reduction, disruption of Purkinje cell layer, cellular degeneration, reduction in NO, CAT and SOD activities. However, these changes were ameliorated when co-administered with MO. Conclusion: The anti-oxidative property of Moringa oleifera is responsible for its ameliorative effect in cuprizone neurotoxicity.
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    Moringa Oleifera is protective against microarchitectural and neurochemical changes associated with cuprizone-induced pre-frontal cortex neurotoxicity in female Wistar rats
    (Neuroscience Society of Nigeria, 2018) Omotoso G.O.; Gbadamosi I.T.; Akinlolu A.A.; Ameen M.O.; Kadir R.E.; Jaji-Sulaimon R.; Abdulwahab A.B.; Kolo R.M.
    Cuprizone administration causes selective damage to axonal myelin sheath and has been used to model demyelinating diseases in neuroscience research. This study aimed at determining the protective effects of Moringa oleifera on cuprizone-induced neurotoxicity in the prefrontal cortex (PFC). Sixteen adult female Wistar rats were procured and grouped into 4: Group A was given normal saline, Group B received 0.4% cuprizone diet, Group C was administered with 1.875 mg/ml of Moringa oleifera and Group D received a combination of 0.4% cuprizone diet and 1.875 mg/ml of Moringa oleifera. All the groups were treated orally for 35 consecutive days after which they were sacrificed. Thereafter the PFC was processed for histological demonstration, while tissue homogenate was used to assay the activity of superoxide dismutase (SOD). Cuprizone administration caused significant reduction in body weight and SOD activities. It also caused an alteration in the microarchitecture and Nissl profile of the PFC. Moringa oleifera intervention led to restoration of body weight, SOD levels, Nissl profile and the histology of the PFC. The use of preparations of Moringa oleifera, especially the leaf-component, could offer some protective measures to individuals suffering from demyelinating conditions, especially in addressing the associated weight changes and frontocortical dysfunction.
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    Prenatal exposure to gestational nicotine before neurulation is detrimental to neurodevelopment of Wistar rats’ offspring
    (Universiti Sains Malaysia, Kelantan, 2018) Omotoso G.O.; Kadir R.E.; Sulaimon F.A.; Jaji-Sulaimon R.; Gbadamosi I.T.
    Background and aim: This study aimed to determine the effect of gestational nicotine exposure before neurodevelopment on the morphology and histology of the prefrontal cortex (PFC) in rats. Methodology: Adult female Wistar rats were time-mated and grouped into three categories: (a) control–given 0.1 mL of normal saline, (b) low-dose nicotine–given 6.88 mg/ kg/d/0.05 mL, and (c) high-dose nicotine–given 13.76 mg/kg/d/0.1 mL in two divided doses. Treatment was given intraperitoneally from gestational days 2 to 6. On postnatal day 15 (P15), the pups were separated from their mothers, anaesthetised and sacrificed, followed by intracardial perfusion with 4% paraformaldehyde. PFC was excised from the brain and processed for tissue histology, histochemistry, and morphology of brain cells. Results: Gestational nicotine exposure during the first week of gestation in rats significantly reduced birth weights in nicotine-treated groups compared with control; it, however, accelerated body weights, altered neuronal morphology, and elevated astrocytic count significantly, while oligodendroglial count was slightly increased in the PFC of juvenile rats examined at P15. Conclusion: These alterations revealed that gestational nicotine exposure before the commencement of the cellular processes involved in brain development negatively affects neurodevelopment, and this could result in neurological dysfunctions in later life.