Browsing by Author "Olugbenga Akinola"

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    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 Amin
    This 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.
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    Mechanisms underpinning Carpolobia lutea G. Don ethanol extract’s neurorestorative and antipsychotic-like activities in an NMDA receptor antagonist model of schizophrenia
    (Journal of Ethnopharmacology, 2023-01-30) Noah A Omeiza; Adewale Bakre; Benneth Ben-Azu; Abimbola A. Sowunmi; Abdulrahim Halimat A; Joseph Chimezie; Sodiq O Lawal; Olusegun G Adebayo; Abdullateef I Alagbonsi; Olugbenga Akinola; Amos O Abolaji; Adegbuyi O. Aderibigbe
    Ethnopharmacological relevance: Persistent ketamine insults to the central nervous system block NMDA receptors and disrupt putative neurotransmission, oxido–nitrosative, and inflammatory pathways, resulting in schizophrenia-like symptoms in animals. Previously, the ethnomedicinal benefits of Carpolobia lutea against insomnia, migraine headache, and insanity has been documented, but the mechanisms of action remain incomplete. Aim of the study: Presently, we explored the neuro-therapeutic role of Carpolobia lutea ethanol extract (C. lutea) in ketamine-induced schizophrenia-like symptoms in mice. Materials and methods: Sixty-four male Swiss (22 ± 2 g) mice were randomly assigned into eight groups (n = 8/ group) and exposed to a reversal ketamine model of schizophrenia. For 14 days, either distilled water (10 mL/kg; p.o.) or ketamine (20 mg/kg; i.p.) was administered, following possible reversal treatments with C. lutea (100, 200, 400, and 800 mg/kg; p.o.), haloperidol (1 mg/kg, p.o.), or clozapine (5 mg/kg; p.o.) beginning on days 8–14. During the experiment, a battery of behavioral characterizations defining schizophrenia-like symptoms were obtained using ANY-maze software, followed by neurochemical, oxido-inflammatory and histological as- sessments in the mice brains. Results: A 7-day reversal treatment with C. lutea reversed predictors of positive, negative and cognitive symptoms of schizophrenia. C. lutea also mitigated ketamine-induced neurochemical derangements as evidenced by mod- ulations of dopamine, glutamate, norepinephrine and serotonin neurotransmission. Also, the increased acetyl- cholinesterase activity, malondialdehyde nitrite, interleukin-6 and tumor necrosis-factor-α concentrations were reversed by C. lutea accompanied with elevated levels of catalase, superoxide dismutase and reduced glutathione. Furthermore, C. lutea reversed ketamine-induced neuronal alterations in the prefrontal cortex, hippocampus and cerebellum sections of the brain. Conclusion: These findings suggest that C. lutea reverses the cardinal symptoms of ketamine-induced schizo- phrenia in a dose-dependent fashion by modulating the oxido-inflammatory and neurotransmitter-related mechanisms.