Browsing by Author "Gbadamosi, I.T."

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    Kolaviron ameliorates histomorphological changes associated with Cuprizone-induced CerebellarDamage
    (2017) Omotoso, G.O.; Olajide, O.J.; Gbadamosi, I.T.; Suleiman, F.A.; Oladimeji, J.O
    Cuprizone is a copper chelator and a drug of choice in studing demyelination/remyelination in the central nervous system. This study assessed the effect of Kolaviron, on cuprizone-induced damage to the cerebellum of Wistar rat. Twenty-four adult male Wistar rats were grouped into 5: Group A received 0.5 ml of normal saline for 6 weeks; Group B received 0.5 ml of corn oil for 6 weeks; Group C was treated with 0.2% of cuprizone for 3 weeks followed by treatment with 200 mg/kg of Kolaviron for another 3 weeks; Group D received 200 mg/kg Kolaviron for 3 weeks followed by 0.2% cuprizone from another 3 weeks; while Group E received 0.2% cuprizone for 6 weeks. Meanwhile, 0.5 ml of corn oil was used as a vehicle for Kolaviron. The body and brain weight of the rats showed significant decrease in all treated groups when compared to the control groups. Histological demonstration showed varying degrees of architectural distortions, including depletion of Nissl bodies, disruption of cortical cell layers and depletion of myelin, which were more pronounced in the cerebellar cortex of cuprizone-treated rats. Kolaviron offered mild cytoprotection to the cerebellar histomorphology of cuprizone-treated rats. Further studies would ascertain the effectiveness of Kolaviron in mitigating cerebellar lesions in well-established demyelination.
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    Moringa oleifera attenuates biochemical and histological changes associated with the pancreas in nicotine-treated rats.
    (2018) Omotoso, G.O.; Adunmo, G.O.; Ojulari, L.S.; Olawuyi, T.S.; Lewu, S.F.; Jaji-Sulaimon, R.; Sulaimon, F.A.; Gbadamosi, I.T.; Onoja, P.
    Objective: The study was undertaken in order to evaluate the beneficial potential of Moringa oleifera, in nicotine-induced pancreatic injury. Method: Forty-five adult female albino rats were divided into 5 groups A-E, each group having nine rats. Group Areceived normal saline; group B received 6.88 mg/kg of nicotine intraperitoneally (i.p); group C received 6.88 mg/kg of nicotine i.p. and 200 mg/kg of Moringa oleifera leaf powder dissolved in 2 ml of normal saline (orally); group D received 13.76 mg/kg of nicotine i.p., while group E received 13.76 mg/kg of nicotine i.p. and 200 mg/kg of Moringa oleifera leaf powder dissolved in 2 ml of normal saline (orally). Treatment was for 8 days and the rats were sacrificed after 24 hours of termination of study. Intracardial blood specimens were obtained to analyse blood glucose, while the pancreas was excised and either fixed in 4% paraformaldehyde for histology or sucrose solution and homogenised for biochemical analysis of lactate dehydrogenase (LDH) and glucose-6-phosphate dehydrogenase (G-6-PDH) enzymes. Results: In comparison with the Control, animals treated with low dose of nicotine with or without Moringa oleifera and those treated with high dose of nicotine plus Moringa oleifera had reduction in body weights (p>0.05), while marked reduction in pancreatic weights was noted in low dose nicotine (p<0.05) and both nicotine groups co-treated with Moringa oleifera (p<0.05). There were no significant changes in the levels of blood glucose and pancreatic G-6-PDH levels, while significant reduction occurred in pancreatic LDH levels in nicotine-treated rats (p<0.05). However, LDH improved following co administration with Moringa oleifera. Observation of the histology of the pancreas revealed atrophy of intercalated ducts, poorly delineated and disintegrating islet of Langerhans in animals treated with the higher dose of nicotine, while changes in pancreatic tissue in animals co-treated with Moringa oleifera were not as severe as the nicotine-treated animals. Conclusion: Moringa oleifera leaf decoction minimally ameliorates morphological and biochemical changes associated with nicotine-induced pancreatic damage.