Browsing by Author "Abdulbasit Amin"
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Item Dichlorvos Induced AChE Inhibition in Discrete Brain Regions and the Neuro-Cognitive Implications: Ameliorative Effect of Nigella Sativa(2018-05-13) Imam Aminu; Adebayo Muhammad; Abdulmajeed Wahab Imam; Alli-Oluwafuyi Abdulmusawir; Abdulbasit Amin; Ibrahim Abdulmumin; Gwadabe Sadiya; NiyiAbdulGafar PopoolaBackground: 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 signi icant. 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 neuro architectures. 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.Item Effect of intranasal insulin on peripheral glucose profile in dexamethasone-induced insulin resistance in Wistar rats(Published by Elsevier, Netherlands, 2018-12) Anoka A. Njan; Chloe O. Fatigun; Abdul-Musawwir Alli-Oluwafuyi; Olufunke E. Olorundare; Saheed O. Afolabi; Olugbenga Akinola; Abdulbasit AminThis study evaluates the therapeutic potential of intranasal insulin (INI) in dexamethasone-induced insulin resistance in Wistar rats. In the first phase of the study, thirteen, healthy, untreated male Wistar rats were divided into 2 groups and administered either vehicle (0.9% Normal saline, 20 µl) or insulin (2 IU) intranasally to assess intranasal delivery of insulin in brain. In the second phase of experiments, to evaluate the acute effects of intranasal insulin on peripheral blood glucose, intranasal or intraperitoneal insulin was co-administered with or without dexamethasone 10 mg/kg to 26 male Wistar rats and blood glucose monitored. To evaluate effect of intranasal insulin in peripheral metabolic disease model, insulin or vehicle was administered via intranasal or intraperitoneal (IP) route to control or dexamethasone (Dex)-treated (0.5 mg/kg, IP) female Wistar rats for seven consecutive days. Twenty-four hours after last dose, trunk blood was collected via cardiac puncture. Biochemical assay of glucose, lipid and insulin was performed on serum while enzyme activity – glucokinase and glucose-6-phosphatase (G6Pase) or lactate dehydrogenase (LDH) and glucose-6-phosphate dehydrogenase (G6PDH) were assayed from liver and brain homogenates respectively. Acute intranasal but not intraperitoneal insulin elevated brain insulin after 30 min. In animals administered single dose of 10 mg/kg dexamethasone, intranasal and intraperitoneal insulin lowered blood glucose within one hour. However, only the former’s effect was maintained at the 3rd and fourth hour. Dex-induced hyperglycemia was associated with increased hepatic glucose-6-phosphatase activity and decreased high-density lipoprotein (HDL), these effect were attenuated by subchronic (INI) administration. Also INI did not induce oxidative stress in the brain which suggests no brain damage during the period of study. Subchronic administration of INI was able to reduce the effect of Dex-induced hyperglycemia that is associated with increased hepatic glucose-6-phosphatase activity and decreased high-density lipoprotein (HDL) without damage to the brain. We demonstrate the potential of brain targeting with intranasal insulin in a rat model of insulin resistance and peripheral metabolic disease.