Browsing by Author "Olajide, OJ"
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Item Kolaviron protects the prefrontal cortex and hippocampus against histomorphological and neurobehavioral changes in cuprizone model of multiple sclerosis.(Malaysian Journal of Medical Sciences, 2018) Omotoso, Gabriel Olaiya; Olajide, OJ; Gbadamosi, IT; Rasheed, MA; Izuogu, CTBackground and Aim: This study explored the efficacy of kolaviron (kv)-a biflavonoid complex isolated from the seeds of Garcinia kola in protecting against Cuprizone (CPZ)-induced demyelination in both prefrontal cortex and hippocampus of Wistar rats. Methodology: Thirty rats were treated to receive (A) 0.5 ml PBS (Control); (B) 0.5 ml corn oil; (C) 0.2% CPZ; (D) 0.2% CPZ and 200 mg/kg of kv and (E) a combination of 200 mg/kg of kv and 0.2% CPZ for 6 weeks each. Rats were assessed for exploratory functions and anxiety-like behaviour before being euthanised and perfused transcardially with 4% paraformaldehyde. Prefrontal and hippocampal thin sections were stained in H&E and cresyl fast violet stains. Results : CPZ-induced demyelination resulted in behavioural impairment as seen by reduced exploratory activities, rearing behaviour, stretch attend posture, center square entry and anxiogenic characteristics. Furthermore, degenerative changes including pyknosis, karyorrhexis, neuronal hypertrophy and reduced Nissl integrity were seen in response to CPZ administration compared to control. However, rats treated with kv before or after CPZ administration showed significant improvement in behavioural outcomes and comparatively normal cytoarchitectural profile in neural tissues. Conclusion: This study showed that kv provides protective roles against CPZ-induced neurotoxicity through prevention of ribosomal protein degradation.Item Moringa oleifera phytochemicals protect the brain against experimental nicotine-induced neurobehavioural disturbances and cerebellar degeneration.(Pathophysiology, 2018) Omotoso, Gabriel Olaiya; Gbadamosi, IT; Olajide, OJ; Dada-Habeeb, SO; Arogundade, TT; Yawson, EONicotine is a neuro-stimulant that has been implicated in the pathophysiology of many brain diseases.The need to prevent or alleviate the resulting dysfunction is therefore paramount, which has also given way to the use of medicinal plants in the management of brain conditions. This study was designed to determine the histomorphological and neurobehavioural changes in the cerebellum of Wistar rats fol-lowing nicotine insult and how such injuries respond to Moringa intervention. Twenty-four adult male Wistar rats were divided into 4 groups. Group A and B were orally treated with normal saline and Moringa oleifera respectively for twenty-eight days; Group C was treated with nicotine while group D was treated orally with Moringa oleifera and intraperitoneally with nicotine for twenty-eight days. Animals were subjected to the open field test on the last day of treatment. 24 h after last day treatment, the animals were anesthetized and perfusion fixation was carried out. The cerebellum was excised and post-fixed in 4%paraformaldehyde and thereafter put through routine histological procedures. Results revealed cytoarchitectural distortion and extreme chromatolysis in neuronal cells of the cerebellar cortical layers in the nicotine-treated group. The Purkinje cells of the cerebellum of animals in this group were degenerated.There were also reduced locomotor activities in the group. Moringa was able to prevent the chromatolysis, distortion of the cerebellar cortical cells and neurobehavioural deficit. Our result suggests that Moringa oleifera could prevent nicotine-induced cerebellar injury in Wistar rats,Item Moringa protects against nicotine-induced morphological and oxidative damage in the frontal cortex of Wistar rats(Anatomy, 2016) Gbadamosi, IT; Omotoso, Gabriel Olaiya; Olajide, OJ; Dada-Habeeb, SO; Arogundade, TTThe use of nicotine-containing substances has been implicated in oxidative-induced neuronal damage in several neurological dysfunctions. This study assessed the antioxidant potentials of Moringa tea on the frontal cortex of Wistar rats. Twenty female Wistar rats were divided into 4 groups of 5 animals each. Group A (control) received normal saline, Group B received 5.71 mg/kg of Moringa tea, Group C was treated with 13.76 mg/kg nicotine, while Group D received 5.71 mg/kg of Moringa tea and 13.76 mg/kg nicotine, for 21 days. Homogenate of excised frontal cortex of rats obtained on day 22 was used to assess the level of malondialdehyde, catalase, superoxide dismutase and glutathione peroxidase, while histological sections were stained with Heamatoxylin and Eosin. Results showed increased activities of malondialdehyde and catalase in group C and a slight increase in group D compared with the Control, while the activity of superoxide dismutase and glutathione peroxidase was reduced. The histological sections showed a normal architecture of the frontal cortex of rats treated with Moringa tea, but disrupted in the group treated with Moringa tea and nicotine and further distortion in those that received nicotine only, when compared with the control group. The results suggest that Moringa tea may reduce the oxidative stress associated with nicotine consumption and limit the extent of structural damage in the frontal cortex of Wistar rats.Item uprizone toxicity and Garcinia kola biflavonoid complex activity on hippocampal morphology and neurobehaviour(Heliyon, Elsevier, 2019-02-26) Omotoso, GO; Olajide, OJ; Gbadamosi, IT; Adebayo, JO; Enaibe, BU; Akinola, OB; Owoyele, BVCuprizone-induced neurotoxicity has been employed to study the biology of remyelination in experimental models of multiple sclerosis. This study was aimed at determining the role of kolaviron, a biflavonoid from Garcinia kola, in mitigating the damaging effects of cuprizone on behaviour and the hippocampus. Twenty-four male albino mice aged 6–8 weeks were categorised into 4 equal groups: Group A (Control) received regular diet; Group B received 200 mg/kg/d of kolaviron in addition to their regular diet; Group C received 0.2% cuprizone diet only, while Group D received both kolaviron and cuprizone diet. The treatment lasted for 35 days after which behavioural tests (Morris water maze, Y maze and open field tests) were conducted and brain tissues were processed for histology, histochemistry (Nissl staining), immunohistochemistry (glial fibrillary acidic protein) and biochemistry (malondialdehyde, superoxide dismutase and glutathione peroxidase). Results showed that cuprizone toxicity led to weight loss, impairment in memory and exploratory drive, oxidative stress, chromatolysis and reactive astrocytosis; meanwhile administration of kolaviron prevented cuprizone-induced weight loss, memory decline, oxidative stress and neuromorphological alterations. In conclusion, administration of kolaviron might be useful in limiting the effects of cuprizone toxicity on the morphology and functions of the hippocampus.