Browsing by Author "Alli-Oluwafuyi, A."

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    Dichlorvos Induced AChE Inhibition in Discrete Brain Regions and the Neuro-Cognitive Implications: Ameliorative Effect of Nigella Sativa.
    (Arak University of Medical Sciences in collaboration with the Iranian Society of Toxicology., 2017) Imam, A.; Adeboye, M. A. N.; Abdulmajeed, W. I.; Alli-Oluwafuyi, A.; Amin, A.; Ibrahim, A.; Gwadabe, S.; Poopola, N. A.
    Background: There has been a rise in accidental poisoning cases resulting from the indiscriminate use and exposure to Dichlorvos (DDVP), especially in developing countries, and no antidote with satisfactory efficacy is currently available. Thus, we investigated the AChE reactivation potential of Nigella sativa oil (NSO) following DDVP induced AChE inhibition patterns in the brain and the associated cognitive implications. Methods: Fourty Wistar rats were randomly divided into four groups of 10 each.; The controls were administered PBS (1 ml/kg); DDVP (8.8 mg/kg) was given to the experimental group I; while DDVP+NSO (8.8 mg/kg + 1 ml/kg) and NSO (1 ml/kg) was administered orally to the experimental groups II and III respectively. All treatments lasted for 14 consecutive days. Morris Water Maze (MWM) paradigm was used to assess the working memory, then rats were euthanized, the brain excised, three brains were fixed for histological examination (Nissl staining), and the other seven brains were homogenized for AChE activity and Ca2+ concentrations. Data were analyzed statistically, using ANOVA method and P values of ≤0.05 was considered as significant. Results: In this study, DDVP differentially inhibited AChE activities in various brain regions: cerebellum (86.1%), hippocampus (40.6%), frontal cortex (33.2%), medulla (21.5%), spinal cord (14.8%), and occipital cortex (8.9%). It reduced Ca2+ concentration, but had no effect on the delayed escape latency in the MWM, nor impaired the neuroarchitectures. NSO caused increased AChE activities, Ca2+ concentration and reduced escape latency, and improved histologic architectures. Conclusion: We concluded that NSO reactivated DDVP-induced AChE inhibition and improved memory indices, thus, it may serve as a potential treatment in the management of DDVP poisoning cases.
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    Hepatoprotective effect of tryptophan in Carbontetrachloride-induced hepatotoxicity in male wistar rats
    (Society of Basic and Applied Physiology, Ahmedabad, India. Available, 2021) Ayinde T.O,; Olayaki L.A.,; Ojulari, L.S.,; Oluwasola A.,; Abdulraheem H.A.; Lawal, A.Z. &; Alli-Oluwafuyi, A.
    In the present study, tryptophan was evaluated for its hepatoprotective effects against carbontetrachloride-induced hepatocellular injury in rats. Hepatotoxicity was induced in male Sprague-Dawley rats by intraperitoneal injection of CCl4 (4ml/kg) in olive oil (1:1). Tryptophan at doses of 100mg/kg and 200mg/kg was administered orally for 28 days. The hepatoprotective effect of tryptophan was evaluated by the assay of biochemical parameters viz.: alanine aminotransaminase (ALT), aspartate aminotransaminase (AST), alkaline phosphatase (ALP), total protein, albumin and lipid peroxidation. Tryptophan produced a dose-dependent significant increase (p<0.001) in serum ALP (41% & 60%), a dose-dependent decrease (p<0.001) in serum Malondialdehyde (61% & 65%), and a significant increase (p<0.001) in levels of serum protein and serum albumin, in CCl4induced hepatotoxic rats, following administration of 100 mg/kg bwand 200 mg/kg bw, respectively. The toxic effect of CCl4 in tryptophan treated groups was controlled significantly by restoration of the levels of enzymes, total protein and albumin as compared to the CCl4 treated groups. The results suggest that tryptophan is able to significantly alleviate the hepatotoxicity induced by CCl4 and may be attributed to the antioxidant property of tryptophan.
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    Hepatoprotective Effect of Tryptophan in Carbontetrachloride-Induced Hepatotoxicity in Male Wistar Rats.
    (Society of Basic and Applied Physiology, 2021) Ayinde, T.O.,; Olayaki, L.A.,; Ojulari, L.S.,; Oluwasola, A.,; Abdulraheem, H.A.,; Lawal, A.Z.,; Alli-Oluwafuyi, A.
    In the present study, tryptophan was evaluated for its hepatoprotective effects against carbontetrachloride-induced hepatocellular injury in rats. Hepatotoxicity was induced in male SpragueDawley rats by intraperitoneal injection of CCl4 (4ml/kg) in olive oil (1:1). Tryptophan at doses of 100mg/kg and 200mg/kg was administered orally for 28 days. The hepatoprotective effect of tryptophan was evaluated by the assay of biochemical parameters viz.: alanine aminotransaminase (ALT), aspartate aminotransaminase (AST), alkaline phosphatase (ALP), total protein, albumin and lipid peroxidation. Tryptophan produced a dose-dependent significant increase (p<0.001) in serum ALP (41% & 60%), a dose-dependent decrease (p<0.001) in serum Malondialdehyde (61% & 65%), and a significant increase (p<0.001) in levels of serum protein and serum albumin, in CCl4induced hepatotoxic rats, following administration of 100 mg/kg bwand 200 mg/kg bw, respectively. The toxic effect of CCl4 in tryptophan treated groups was controlled significantly by restoration of the levels of enzymes, total protein and albumin as compared to the CCl4 treated groups. The results suggest that tryptophan is able to significantly alleviate the hepatotoxicity induced by CCl4 and may be attributed to the antioxidant property of tryptophan.
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    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.; Sheu, 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.