Browsing by Author "Adegbuyi O. Aderibigbe"

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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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    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.
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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.