Browsing by Author "Alli-Oluwafuyi, A.,"

Now showing 1 - 2 of 2
  • Item
    Black seed oil ameliorated scopolamine-induced memory dysfunction and cortico-hippocampal neural alterations in male Wistar rats.
    (Bulletin of Faculty of Pharmacy,, 2016) Imam, A.,; Ajao, M, S.,; Ajibola, M.I.,; Amin, A.,; Abdulmajeed, W.I.,; Lawal, A.Z.,; Alli-Oluwafuyi, A.,; Akinola, O.B.,; Oyewopo, A.O.,; Olajide, O.J. &; Adana, M.Y.
    This study was conducted to evaluate cognitive enhancing effect and ameliorative effects of black seed oil in scopolamine induced rat model of cognitive impairment. These effects were investigated on scopolamine-induced dementia model in Morris water maze test (MWM) and Y maze test. The hippocampal histoarchitectural responses to scopolamine and Nigella sativa oil were also examined. Scopolamine (1 mg/kg ip) was given to induce dementia, followed by oral administration of BSO (1 ml/kg) for 14 consecutive days. MWM and Y-maze paradigms were used to assess hippocampal and frontal dependent memory respectively, thereafter the rats were sacrificed and brains were removed for histopathologic studies. Scopolamine resulted in memory impairment, by delayed latency in the MWM, reduced percentage alternation in the Y maze that was coupled by alterations in the cortico-hippocampal neurons. Posttreatment of rats with BSO mitigated scopolamine-induced amnesia, by reducing latency period and increasing percentage alternation and histological changes. The observed anti-amnestic effect of BSO m
  • Item
    Impaired cognitive performance and metabolic disturbance in streptozotocin-nicotinamide induced type 2 diabetes mellitus and the protective effect of Nigerian propolis
    (Nigerian Journal of Neuroscience, 2016) Amin, A.,; Saliu, H.,; Solomon, E.O.,; Shehu, T.,; Imam, A.,; Abdulmajeed, W.I.,; Alli-Oluwafuyi, A.,; Ibrahim, R.B.,; Owoyele, B.V.
    Defects in insulin signaling and oxidative stress are implicated in cognitive dysfunction in diabetes. This study evaluated the effects of propolis on cognitive impairment in streptozotocin-nicotinamide model of type 2 diabetes mellitus in Wistar rats. Diabetes was induced by single intraperitonieal administration of streptozotocin (65 mg/kg) 15 min after nicotinamide (110 mg/kg) had been adminstered. Diabetic animals were treated with glibenclamide (5 mg/kg), propolis (200 and 300 mg/kg), or normal saline for 4 weeks after which spatial memory was assessed with the Morris’ water maze (MWM). At the end of the study the animals were euthanized and blood collected via cardiac puncture while the brain was homogenized. Insulin was assayed from plasma while malondialdehyde (MDA), superoxide dismutase (SOD), gluthatione (GSH) and catalase were assayed from brain homogenate. Homeostatic model assessment (HOMA) was used as marker for insulin resistance. Significant rise in blood glucose, plasma insulin, and brain MDA (P < 0.05) with reduction in SOD, GSH, and catalase levels were observed in the diabetic group. Treatment with 200 and 300 mg/kg propolis and glibenclamide significantly decreased blood glucose, plasma insulin, and MDA (P < 0.05) and increased brain levels of SOD, GSH and catalase. Propolis (200 and 300 mg/kg) also significantly (P < 0.05) decreased escape latency in the MWM in comparison to the diabetic group. Nigerian propolis thus seems to protect against impaired cognitive performance in experimental diabetes mellitus.