Browsing by Author "Noah A. Omeiza"

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    Abstracts Presented at the 16th Conference of the Neuroscience Society of Nigeria Prosopis africana seeds aqueous extract modulates brain and serum lipid profiles of female Wistar...
    (Nig. J. Neurosci., 2019) Abdulrahim Halimat A.; Adeniran S. Adekunle; Adesola I. R. Abioye; Abdulrazaq B. Nafiu; Abdul-rahuf A. Feyitimi; Noah A. Omeiza; Benedict B. Siaka; Tavershima M. Ateh
    Lipid profile and atherogenic index have been shown to be substantial predictors for metabolic disturbances and challenges such as cost and adverse effects make investigation on plants and their bioactive components indispensable. This study seeks to evaluate the pharmacological potential of Prosopis Africana (PA) seeds aqueous extract on lipid metabolism in female Wistar rats. The rats (200-230g; n=10) were exposed to PA at varying doses (500 mg/kg b.w., p.o) or (1000 mg/kg b.w., p.o) once per day for thirty days. Control animals (n=5) were exposed to 0.2 ml/kg b.w/day physiological saline for the same period via intragastric gavages. Blood and brain tissue supernatants were collected for biochemical assays. The result showed a significant (p<0.05) influences of PA on total cholesterol, low density lipoprotein, high density lipoprotein concentrations in both serum and brain tissue; cardiovascular risk ratios and atherogenic index were being raised when com- pare PA-treated to control. Meanwhile, PA at 500 and 1000 mg/kg showed insignificant (p˃0.05) decrease in serum triglycerides and very low density lipoprotein. These findings indicate that both PA regimen potentially increased serum lipids (TC and LDL-C) along with reduced HDL-C reflecting the characteristic dyslipidemic effect and their vascular hemodynamic disturbances which may favour plaque formation and promotes risk of atherosclerosis. Furthermore, PA dosages in brain homogenates modulate the lipid concentration (lowers TC and LDL-C, increases TG and HDL-C). Aqueous extract PA seeds enhanced transport of cholesterol from nervous tissues to the liver for further metabolic needs. Therefore PA possessed cardioprotective and neuroprotective properties.
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    Diosgenin reverses posttraumatic stress disorder in mice by augmenting neurochemical release and inhibiting HPA axis dysfunction, oxidative stress, and neuroinflammation
    (Journal of Affective Disorders Reports, 2024-07) Benneth Ben-Azu; Olusegun G. Adebayo; Adaeze Adebesin; Kenneth C. Oparaji; Vivian O. Ojiakor; Gift C. Pender; Bensandy O. Odeghe; Noah A. Omeiza; Abdulrahim Halimat A; Vivian Ezieshi; Glory Ighosotu; Emmanuel Omo-Odudu; Ekene I. Monye
    Post-traumatic stress disorder (PTSD) is a mental disorder linked to neurochemical, hypothalamic-pituitary- adrenal (HPA)-axis dysregulations, inflammatory and pro-oxidant challenges in response to traumatic events. It is one of the leading causes of neurocognitive declines, hence prompting the need for a pharmacological intervention. However, the impact of diosgenin, a naturally occurring steroidal saponin with adaptogenic-like action, on PTSD-induced neuropsychiatric disturbances and its underlying mechanisms are unknown. In this study, we investigated the outcome of diosgenin treatment in a multimodal traumatic, single prolonged stress (SPS)-induced PTSD in mice. Following the SPS-induced 7 days of PTSD, mice (n = 9) were thereafter treated with diosgenin (25 and 50 mg/kg) or fluoxetine (10 mg/kg) orally from days 8–20 (14 days). Locomotory, cognitive-, depressive- and anxiety-like behaviors were investigated. We assayed for changes in adrenal weight, serum glucose and corticosterone concentrations. Neurochemical, inflammatory, oxido-nitrergic dysfunctions and monoamine oxidase-B and acetylcholinesterase activities, were measured in the striatum, prefrontal-cortex and hippocampus. The results revealed that the SPS challenge inhibited locomotor, spatial/non-spatial memory functions, increased anxiety and depressive-like features, which were reversed by diosgenin. Diosgenin reduced SPS-induced increased monoamine oxidase-B, acetylcholinesterase activities, TNF-α, IL-6, malondialdehyde and nitrite levels in the striatum, prefrontal-cortex and hippocampus. Antioxidants such as glutathione, superoxide- dismutase, and catalase levels in SPS-mice brains were increased by diosgenin. Moreover, diosgenin attenuated SPS-induced hyper-HPA-axis mediation of PTSD by decreasing serum corticosterone, glucose levels and adrenal gland hypertrophy. Herewith, we suggest that diosgenin convenes adaptogenic-like protection against mice exposed to PTSD by enhancing antioxidant machinery, neurochemical modulations, and inhibition of oxido- nitrergic, inflammatory, and HPA-axis dysfunctions.
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    Dissecting the antidepressant efect of troxerutin: modulation of neuroinfammatory and oxidative stress biomarkers in lipopolysaccharide‐treated mice
    (Naunyn-Schmiedeberg's Archives of Pharmacology, 2024-06-29) Abimbola A. Sowunmi; Noah A. Omeiza; Adewale Bakre; Halimat A. Abdulrahim; Adegbuyi O. Aderibigbe
    The role of neuroinfammation in the pathogenesis of depression has prompted the search for new antidepressants. Troxerutin, a biofavonoid with anti-infammatory and antioxidant properties, has shown promise, but its impact on neurobehavioral functions remains poorly understood. This study aimed to investigate the antidepressant potential of troxerutin and its efect on the neuroinfammatory response. Here, we exposed male Swiss mice (n=5/group) to various treatments, including naive and negative controls receiving distilled water, troxerutin-treated groups administered at diferent doses (10, 20, 40 mg/kg, i.p.), and an imipramine-treated group (25 mg/kg, i.p.). After seven days of treatment, with the exception of the naive group, mice were administered a single dose of lipopolysaccharide (LPS, 0.83 mg/kg). Behavioral evaluations, consisting of the novelty-suppressed feeding (NSF) test, forced swim test (FST), and open feld test (OFT), were conducted. Additionally, brain samples were collected for biochemical and immunohistochemical analyses. Troxerutin signifcantly reduced immobility time in the FST and mitigated behavioral defcits in the NSF test. Additionally, troxerutin increased glutathione (GSH) and superoxide dismutase (SOD) levels while reducing nitrite, malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interferon-gamma (IFN-γ) levels compared to the negative control. Immunohistochemistry analysis revealed decreased expression of inducible nitric oxide synthase (iNOS) and nuclear factor-kappa B (NF-κB) in troxerutin- treated mice. Overall, these fndings suggest that troxerutin exerts signifcant antidepressive-like efects, likely mediated by its anti-infammatory and antioxidant mechanisms. The reduction in neuroinfammatory and oxidative stress biomarkers, along with the improvement in behavioral outcomes, underscores troxerutin's potential as a therapeutic agent for depression.
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    Pretreatment with Carpolobia lutea ethanol extract prevents schizophrenia-like behavior in mice models of psychosis
    (Journal of Ethnopharmacology3 June 2022, 2022-06-03) Noah A. Omeiza; Adewale G. Bakre; Abdulrahim Halimat A.; Happy Isibor; Precious U. Ezurike; Abimbola A. Sowunmi; Benneth Ben-Azu; Adegbuyi O. Aderibigbe
    Ethnopharmacological relevance: Carpolobia lutea decoction is widely used as a phytotherapeutic against central nervous system-related disorders including insomnia, migraine headache, and mental illness in West and Central Tropical Africa. Aim: This study was designed to investigate the antipsychotic activity of Carpolobia lutea (EECL) in mice models of psychosis. Methods: Male Swiss mice (n = 5/group) were given EECL (100, 200, 400, and 800 mg/kg), haloperidol (1 mg/ kg), clozapine (5 mg/kg) and vehicle (10 mL/kg) orally before amphetamine (5 mg/kg)-induced hyper- locomotion and stereotypy, apomorphine (2 mg/kg)-induced stereotypy, or ketamine (10, 30, and 100 mg/kg)- induced hyperlocomotion, enhancement of immobility and cognitive impairment. Results: EECL (200, 400, and 800 mg/kg) prevented amphetamine- and apomorphine-induced stereotypies, as well as reduced hyperlocomotion induced by amphetamine and ketamine, all of which are predictors of positive symptoms. Regardless of the dose administered, EECL prevented the index of negative symptoms induced by ketamine. Furthermore, higher doses of EECL (400 and 800 mg/kg) also prevented ketamine-induced cognitive impairment, a behavioral phenotype of cognitive symptoms. Conclusion: Pretreatment with EECL demonstrated antipsychotic activity in mice, preventing amphetamine-, apomorphine-, and ketamine-induced schizophrenia-like symptoms, with 800 mg/kg being the most effective dose.