Browsing by Author "Sulaimon, F."

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    NR2B-DAPK1-P53 mediated hippocampal cell death following monosodium glutamate ingestion and interventions with luteolin, caffeic-acid, and phoenix dactylifera
    (Published by Nepalese Society of Neurosurgeons, 2022) Ibiyeye, R.; Imam, A.; Adana, M.; Sulaimon, F.; Ajao, M.
    Introduction: Glutamate is the major excitatory neurotransmitter in the brain, but its accumulation potentiates excitotoxicity. In most food seasonings is the monosodium glutamate (MSG), whose over ingestion have been reported with glutamate-like neurotoxicity, thus, this study investigated the efficacy of Phoenix dactylifera and two of its phytochemicals MSG hippocampal toxicity. Materials and Methods: Forty-eight male Wistar rats were randomly allocated to eight groups of six rats each (n=6). The control received normal saline, group 2 received 4 g/kg MSG, groups 3 to 5 received 4 g/kg MSG followed by 100 mg/kg caffeic-acid, 100 mg/kg luteolin and 500 mg/kg Phoenix dactylifera, while groups 6 to 8 received the above agents first followed by 4 g/kg MSG orally for 21 days. 24 hours after the last ingestion, the rats were euthanized and hippocamapal tissue was removed and processed for GluN2B, DAPK1 and p53 immuno histochemical staining. Results: Repeated MSG ingestions caused high expressions of GluN2B, DAPK1 and p53 in the hippocampus of the exposed rats suggestive of an apoptotic cascades along the NR2B-DAPK1-P53 neuronal death pathway. Pre- or post treatment with caffeic-acid, luteolin or Phoenix dactylifera markedly reduced the hippocampal expressions GluN2B, DAPK1 and p53. Conclusion: Phoenix dactylifera and its flavonoids are capable of downplaying the activities GluN2B, DAPK1 and p53 in MSG toxicity, thereby preventing hippocampal cell death.
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    Phoenix dactylifera and Polyphenols Ameliorated Monosodium Glutamate toxicity in the Dentate Gyrus of Wistar Rats
    (Physiological Society of Nigeria, 2023) Ibiyeye, R.; Sulaimon, F.; Imam, A.; Adana, M.; Okesina, A.; Ajao, M.
    Monosodium glutamate (MSG) has been known to cause neurodegeneration, due to its ability to trigger excitotoxicity, and the hippocampus is one of the most affected regions. Therefore, Phoenix dactylifera (P. dactyliferaa ) and polyphenols were employed in this study to mitigate on the deleterious effect of monosodium glutamate on the dentate gyrus of Wistar rats. Forty-eight male Wistar rats weighing between 120-150g was used for the study. The Wistar rats were grouped into eight, (n=6). Groups 1-8 received 1.6mL/kg normal saline, 4000mg\kg monosodium glutamate for 7-days, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg caffeic-acid for 14-days concurrently, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg P. dactyliferaa for 14-days concurrently, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg luteolin for 14-days concurrently, 100mg\kg. caffeic-acid for 14-days followed by 4000mg\kg monosodium glutamate for 7-days, 100mg\kg P. dactyliferaa for 14-days followed by 4000mg\kg monosodium glutamate for 7-days and 100mg\kg luteolin for 14-days followed by 4000mg\kg monosodium glutamate for 7-days respectively. After the treatments, the rats underwent behavioural test (Y-maze test), and subsequently, the brain tissues were processed for histological (Hematoxylin & Eosin stain) and biochemical (superoxide dismustase, glutathione peroxidase and malondialdehyde) analyses. The activities of P. dactyliferaa and polyphenols ameliorated the deleterious effect of monosodium glutamate, through increased spontaneous alternation of the experimental animals, dominant matured granule cells of the dentate gyrus and modulated the activities of superoxide dismutase, glutathione peroxidase and malondialdehyde in the male Wistar rats. Therefore, this study revealed that P. dactyliferaa and polyphenols ameliorated monosodium glutamate toxicity in the dentate gyrus of Wistar rats.
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    Phoenix dactylifera and polyphenols ameliorated monosodium glutamate toxicity in the dentate gyrus of Wistar rats
    (Physiological Society of Nigeria, 2023) Adana, M. Y.; Ibiyeye, R.; Sulaimon, F.; Imam, A.; Okesina, A.; Ajao, M.
    Monosodium glutamate (MSG) has been known to cause neurodegeneration, due to its ability to trigger excitotoxicity, and the hippocampus is one of the most affected regions. Therefore, Phoenix dactylifera (P. dactyliferaa ) and polyphenols were employed in this study to mitigate on the deleterious effect of monosodium glutamate on the dentate gyrus of Wistar rats. Forty-eight male Wistar rats weighing between 120-150g was used for the study. The Wistar rats were grouped into eight, (n=6). Groups 1-8 received 1.6mL/kg normal saline, 4000mg\kg monosodium glutamate for 7-days, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg caffeic-acid for 14-days concurrently, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg P. dactyliferaa for 14-days concurrently, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg luteolin for 14-days concurrently, 100mg\kg. caffeic-acid for 14-days followed by 4000mg\kg monosodium glutamate for 7-days, 100mg\kg P. dactyliferaa for 14-days followed by 4000mg\kg monosodium glutamate for 7-days and 100mg\kg luteolin for 14-days followed by 4000mg\kg monosodium glutamate for 7-days respectively. After the treatments, the rats underwent behavioural test (Y-maze test), and subsequently, the brain tissues were processed for histological (Hematoxylin & Eosin stain) and biochemical (superoxide dismustase, glutathione peroxidase and malondialdehyde) analyses. The activities of P. dactyliferaa and polyphenols ameliorated the deleterious effect of monosodium glutamate, through increased spontaneous alternation of the experimental animals, dominant matured granule cells of the dentate gyrus and modulated the activities of superoxide dismutase, glutathione peroxidase and malondialdehyde in the male Wistar rats. Therefore, this study revealed that P. dactyliferaa and polyphenols ameliorated monosodium glutamate toxicity in the dentate gyrus of Wistar rats.
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    Prenatal Exposure to Gestational Nicotine before Neurulation is Detrimental to Neurodevelopment of Wistar Rats’ Offspring
    (Penerbit Universiti Sains Malaysia, 2018) Omotoso, G.O.; Kadir, R.E.; Sulaimon, F.; Jaji-Sulaimon, R.; Gbadamosi, I.T
    re before neurodevelopment on the morphology and histology of the prefrontal cortex (PFC) in rats. Methodology: Adult female Wistar rats were time-mated and grouped into three categories: (a) control–given 0.1 mL of normal saline, (b) low-dose nicotine–given 6.88 mg/ kg/d/0.05 mL, and (c) high-dose nicotine–given 13.76 mg/kg/d/0.1 mL in two divided doses. Treatment was given intraperitoneally from gestational days 2 to 6. On postnatal day 15 (P15), the pups were separated from their mothers, anaesthetised and sacrificed, followed by intracardial perfusion with 4% paraformaldehyde. PFC was excised from the brain and processed for tissue histology, histochemistry, and morphology of brain cells. Results: Gestational nicotine exposure during the first week of gestation in rats significantly reduced birth weights in nicotine-treated groups compared with control; it, however, accelerated body weights, altered neuronal morphology, and elevated astrocytic count significantly, while oligodendroglial count was slightly increased in the PFC of juvenile rats examined at P15. Conclusion: These alterations revealed that gestational nicotine exposure before the commencement of the cellular processes involved in brain development negatively affects neurodevelopment, and this could result in neurological dysfunctions in later life.