Browsing by Author "Shehu, M."

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    Exogenous Melatonin Ameliorates Pontine Histoarchitecture and Associated Oxidative Damage in Sodium Fluoride Induced Toxicity
    (2020) Sulaimon, F.A.; Okesina, A.A.; Imam, A.L.; Usman, R.Y.; Ibrahim-Abdulkareem, R.A.; Imam, A.; Adana, M.Y.,; Shehu, M.; Abioye, A.’I.R.; Ayuba, A.I.; Ajao, M.S.
    Background: Sodium fluoride (NaF) is a highly consumed food additive, that is capable of disrupting the activities of several brain areas. It is unclear whether this compound affects the autonomic activities of the brain. Objective: Therefore, this study was designed to investigate the ameliorative potentials of exogenous melatonin on sodium fluoride-induced pontine toxicity in adult male Wistar rats, as melatonin has been implicated to have a high concentration in the cerebrospinal fluid of injured brains. Method: Thirty-two rats were randomly divided into 4 groups (n=8, per group). Groups I, II, III and IV received 0.2 ml of normal saline (NS), 500 ppm of sodium fluoride (NaF) via their drinking water, 10 mg/kg melatonin (MLT), and melatonin with sodium fluoride concurrently (MLT+NaF) respectively for fourteen days. At the end of these treatments, the rats were euthanized and brainstem tissues were excised for histological, histochemical, and biochemical analyses. Results: There were shreds of evidence of DNA fragmentation, vacuolation, dispersion of the Nissl bodies, and axonal disruption in the cells of the basilar pons of the sodium fluoride-treated animals. This was coupled with high concentrations of malondialdehyde and low-level concentrations of glutathione reductase. Melatonin, however, was observed to limit neuronal injury in the cells of the basilar pons in the experimental animals by reducing the extent of cells undergoing process pyknosis, chromatolysis, and demyelination. Also, melatonin was able to reduce the concentration of malondialdehyde and increase glutathione reductase activities in the pons. Conclusion: This study revealed that sodium fluoride injured the pontine histoarchitecture, and induced oxidative damage which were ameliorated by exogenous melatonin treatments.
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    Honey and levodopa comparably preserved substantia nigra pars compacta neurons through the modulation of nuclear factor erythroid 2-related factor 2 signaling pathway in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease model
    (Korean Association of Anatomists, 2024) Sulaimon, F. A.; Ibiyeye, R. Y.; Imam, A.; Oyewole, A. L.; Imam, A. L.; Shehu, M.; Biliaminu, S. A.; Kadir, R. E.; Omotoso, G. O.; Ajao, M. S.
    : Parkinson’s disease (PD) affects about 8.5 million individuals worldwide. Oxidative and inflammatory cascades are implicated in the neurological sequels, that are mostly unresolved in PD treatments. However, proper nutrition offers one of the most effective and least costly ways to decrease the burden of many diseases and their associated risk factors. Moreover, prevention may be the best response to the progressive nature of PD, thus, the therapeutic novelty of honey and levodopa may be prospective. This study aimed to investigate the neuroprotective role of honey and levodopa against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced oxidative stress. Fifty-four adult male Swiss mice were divided into control and PD model groups of 27 mice. Each third of the control mice either received phosphate buffered saline, honey, or levodopa for 21 days. However, each third of the PD models was either pretreated with honey and levodopa or not pretreated. Behavioral studies and euthanasia were conducted 2 and 8 days after MPTP administration respectively. The result showed that there were significantly (P<0.05) higher motor activities in the PD models pretreated with the honey as well as levodopa. furthermore, the pretreatments protected the midbrain against the chromatolysis and astrogliosis induced by MPTP. The expression of antioxidant markers (glutathione [GSH] and nuclear factor erythroid 2-related factor 2 [Nrf2]) was also significantly upregulated in the pretreated PD models. It is thus concluded that honey and levodopa comparably protected the substantia nigra pars compacta neurons against oxidative stress by modulating the Nrf2 signaling molecule thereby increasing GSH level to prevent MPTP-induced oxidative stress.
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    Nigella sativa oil ingestion mitigates aluminum chloride (alcl3) induced cerebellar oxidative, neurogenic damages and impaired motor functions in Wistar rats
    (Association of Anatomical Societies of Africa, 2022) Imam, A.; Sulaimon, F. A.; Shehu, M.; Busari, M.; Oyegbola, C.; Okesina, A. A.; Afodun A. M.; Adana, M. Y.; Ajao, M. S.
    Varying neurological effects, and impairments to motor functions, neurochemistry and neuromorphology have been associated with Aluminium chloride (AlCl3) induced neurotoxicity. This study aims to investigate the efficacy of Nigella sativa oil (NSO) in AlCl3 induced cerebellar toxicity in rats. Thirty-two male Wistar rats were randomly divided into four groups and received: normal saline; 100 mg/kg.bw of AlCl3; 100 mg/kg.bw AlCl3 and 1 ml/kg.bw of NSO; and 1 ml/kg.bw, orally and daily for fourteen days. On the 13th day of the experiment, the rats were each exposed to a single trial of the Open Field Test (OFT), of which line crossing frequency, rearing frequency, and freezing period were recorded as measures of exploratory and locomotive behaviours of the animals. By day 15, the rats were euthanized, their brains were excised, the cerebellum dissected from five brains of each group, and homogenized for biochemical evaluations of nitric oxide (NO) metabolites and total reactive oxygen species (ROS) levels. The remaining three brains in each group were processed for histology and Ki67 immunohistochemistry investigations. The results of this study shows that AlCl3 impaired motor related behaviours in the AlCl3 exposed animals, by significantly reducing the line crossing and rearing frequencies, and increasing the freezing period. This effect was observed to be mitigated in the animal group that received NSO following AlCl3 administration, as the animals showed improved motor behaviours. AlCl3 also caused an increase in the cerebellar activities of NO and ROS, while it depleted Ki67 expressions and caused neurodegenerative-like effects in the cerebellar histoarchitecture of the exposed animals. Intervention with NSO depleted ROS/NO levels and protected the cerebellum from the nitrosative and oxidative stress induced by AlCl3. NSO was also observed to preserve the cerebellar cortex histoarchitecture and neurogenic morphology against the neurodegenerative effect of AlCl3. It can be concluded that NSO, with its high efficacy against oxidative stress and neuroinflammation, is a potent natural therapeutic agent in aluminum and heavy metal neurotoxicity.
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    Thymoquinone ameliorate oxidative stress, GABAergic neuronal depletion and memory impairment through Nrf2/ARE signaling pathway in the dentate gyrus following cypermethrin administration
    (BMC Neuroscience, 2024) Imam, A. L.; Okesina, A. A.; Sulaimon, F. A.; Imam, A.; Ibiyeye, R. Y.; Oyewole, L. A.; Biliaminu, S. A.; Shehu, M.; Alli, A. O.; Omoola, O. O.; Ajao, M.S.
    Background Exposure to chemical toxins, including insecticides, harms bodily organs like the brain. This study examined the neuroprotective of thymoquinone on the cypermethrin’s harmful effects on the histoarchitecture of the dentate gyrus and motor deficit in the dentate gyrus. Methods Forty adult male rats (180–200 g) were randomly divided into 5 groups (n=8 per group). Groups I, II, III, IV, and V received oral administration of 0.5 ml of phosphate-buffered saline, cypermethrin (20 mg/kg), thymoquinone (10 mg/kg), cypermethrin (20 mg/kg)+thymoquinone (5 mg/kg), and cypermethrin (20 mg/kg)+thymoquinone (10 mg/kg) for 14 days respectively. The novel object recognition test that assesses intermediate-term memory was done on days 14 and 21 of the experiment. At the end of these treatments, the animals were euthanized and taken for cytoarchitectural (hematoxylin and eosin; Cresyl violet) and immunohistochemical studies (Nuclear factor erythroid 2-related factor 2 (Nrf2), Parvalbumin, and B-cell lymphoma 2 (Bcl2). Result The study shows that thymoquinone at 5 and 10 mg/kg improved Novelty preference and discrimination index. Thymoquinone enhanced Nissl body integrity, increased GABBAergic interneuron expression, nuclear factor erythroid 2-derived factor 2, and enhanced Bcl-2 expression in the dentate gyrus. It also improved the concentration of nuclear factor erythroid 2-derived factor 2, increased the activities of superoxide dismutase and glutathione, and decreased the concentration of malondialdehyde level against cypermethrin-induced neurotoxicity. Conclusion thymoquinone could be a therapeutic agent against cypermethrin poisoning.