Browsing by Author "Imam, A."

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    Dichlorvos Induced AChE Inhibition in Discrete Brain Regions and the Neuro-Cognitive Implications: Ameliorative Effect of Nigella Sativa.
    (Arak University of Medical Sciences in collaboration with the Iranian Society of Toxicology., 2017) Imam, A.; Adeboye, M. A. N.; Abdulmajeed, W. I.; Alli-Oluwafuyi, A.; Amin, A.; Ibrahim, A.; Gwadabe, S.; Poopola, N. A.
    Background: There has been a rise in accidental poisoning cases resulting from the indiscriminate use and exposure to Dichlorvos (DDVP), especially in developing countries, and no antidote with satisfactory efficacy is currently available. Thus, we investigated the AChE reactivation potential of Nigella sativa oil (NSO) following DDVP induced AChE inhibition patterns in the brain and the associated cognitive implications. Methods: Fourty Wistar rats were randomly divided into four groups of 10 each.; The controls were administered PBS (1 ml/kg); DDVP (8.8 mg/kg) was given to the experimental group I; while DDVP+NSO (8.8 mg/kg + 1 ml/kg) and NSO (1 ml/kg) was administered orally to the experimental groups II and III respectively. All treatments lasted for 14 consecutive days. Morris Water Maze (MWM) paradigm was used to assess the working memory, then rats were euthanized, the brain excised, three brains were fixed for histological examination (Nissl staining), and the other seven brains were homogenized for AChE activity and Ca2+ concentrations. Data were analyzed statistically, using ANOVA method and P values of ≤0.05 was considered as significant. Results: In this study, DDVP differentially inhibited AChE activities in various brain regions: cerebellum (86.1%), hippocampus (40.6%), frontal cortex (33.2%), medulla (21.5%), spinal cord (14.8%), and occipital cortex (8.9%). It reduced Ca2+ concentration, but had no effect on the delayed escape latency in the MWM, nor impaired the neuroarchitectures. NSO caused increased AChE activities, Ca2+ concentration and reduced escape latency, and improved histologic architectures. Conclusion: We concluded that NSO reactivated DDVP-induced AChE inhibition and improved memory indices, thus, it may serve as a potential treatment in the management of DDVP poisoning cases.
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    Dichlorvos induced oxidative and neuronal responses in rats: mitigative efficacy of Nigella sativa (black cumin)
    (Physiological Society of Nigeria, 2018) Adana, M. Y.; Imam, A.; Ogunniyi, A.; Ibrahim, A.; Abdulmajeed, W. I.; Oyewole, L. A.; Lawan, A. H.; Sulaimon, F. A.; Ajao, M. S.
    Poisoning from Organophosphates (OPs), especially Dichlorvos (DDVP) has become endemic due to the increasing use in house hold and agricultural pests control, with most marked effects in the nervous system. However, it is evidenced that natural antioxidants are efficacious against OPs toxicity. Thus, this study investigated the possible antidotal efficacy of Nigella sativa oil (NSO) in Dichlovos (DDVP) induced oxidative and neuronal damages in Wistar rats. DDVP was administered at sub-chronic daily dosage of 8.8 mg/kg.bw for 7 days and a post-administration of NSO at 1 ml/kg.bw for the subsequent 7 days. The rats were euthanized on the 15thday, blood sample collected via cardiac puncture, centrifuged and the plasma used for biochemical analysis of total antioxidant capacity (TAC), reduced glutathione (GSH) and total reactive oxygen species (ROS), while the frontal, occipital and cerebellar cortices and the medulla were removed for histomorphological examinations. The results showed significant (P≤0.05) decrease in plasma TAC and GSH, while a significant (P≤0.05) increase in ROS was recorded, and some vacuolation around the neurons especially in the frontal and cerebellar cortices following DDVP exposure. However, post treatment with NSO was observed to be efficacious in the recovery of the oxidative activities and the neuro-architectural integrities. Thus, it can be concluded that the antioxidant capacity of NSO could be efficacious against OPs induced oxidative damages, especially in dichlorvos accidents.
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    Dichlorvos induced oxidative and neuronal responses in rats; mitigative efficacy of Nigella sativa (black cumin)
    (2018) Imam, A.; Ogunniyi, A.; Ibrahim, A.; Abdulmajeed, W.I.; Oyewole, L.A.; Lawan, A.H.; Sulaimon, F.A.; Adana, M.Y.; Ajao M.S
    Poisoning from Organophosphates (OPs), especially Dichlorvos (DDVP) has become endemic due to the increasing use in house hold and agricultural pests control, with most marked effects in the nervous system. However, it is evidenced that natural antioxidants are efficacious against OPs toxicity. Thus, this study investigated the possible antidotal efficacy of Nigella sativa oil (NSO) in Dichlovos (DDVP) induced oxidative and neuronal damages in Wistar rats. DDVP was administered at sub-chronic daily dosage of 8.8 mg/kg.bw for 7 days and a post-administration of NSO at 1 ml/kg.bw for the subsequent 7 days. The rats were euthanized on the 15thday, blood sample collected via cardiac puncture, centrifuged and the plasma used for biochemical analysis of total antioxidant capacity (TAC), reduced glutathione (GSH) and total reactive oxygen species (ROS), while the frontal, occipital and cerebellar cortices and the medulla were removed for histo morphological examinations. The results showed significant (P≤0.05) decrease in plasma TAC and GSH, while a significant (P≤0.05) increase in ROS was recorded, and some vacuolation around the neurons especially in the frontal and cerebellar cortices following DDVP exposure. However, post treatment with NSO was observed to be efficacious in the recovery of the oxidative activities and the neuro-architectural integrities. Thus, it can be concluded that the antioxidant capacity of NSO could be efficacious against OPs induced oxidative damages, especially in dichlorvos accidents.
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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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    Exogenous melatonin restored the cytoarchitectural integrity and biochemical activities of the cerebrum in sodium fluoride-induced toxicity.
    (Spanish Society of Anatomy and the Mexican Society of Anatomy, 2021) Ibrahim-Abdulkareem, R. A.; Okesina, A. A.; Sulaimon, F. A.; Imam, A.; Yawson, E.; Oluyomi, O.O.; Ajao M.S
    The cerebrum is responsible for motor, sensory and autonomic activities of the human body, and it is believed that fluoride exposure to the biological system can impede these functions. Therefore, it is imperative to introduce melatonin to limit the extent of fluoride toxicity on the cerebrum and understand the mechanism involved in the aforementioned process. Thirty-two rats were randomly selected into 4 groups (n=8, per group). Groups I-IV received oral administration of 0.2ml of normal saline (NS), 500ppm of sodium fluoride (NaF), concurrent administration of sodium fluoride and melatonin (NaF+MLT), and sodium fluoride before melatonin (NaF-MLT) for fourteen days respectively. At the end of these treatments, the rats were euthanized and cerebral tissues were excised for histological, histochemical and biochemical analyses. Sodium fluoride distorted the shapes and size of the cells and caused constriction of the blood vessels, as well as presence of vacuolations in the cells of the pyramidal layer of the cerebral cortex. However, melatonin was able to restore the cytoarchitecture of cells of the pyramidal layer of the cerebral cortex when administered concurrently and after the administration of sodium fluoride (NaF) respectively. Also, melatonin regulated the activities of Superoxide dismutase, Malondialdehyde and Glutathione peroxidase in the cerebrum. Sodium fluoride causes neurodegeneration in the cerebral cortex, and exogenous melatonin can ameliorate the injury caused by sodium fluoride on the cerebral cortex.
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    Hippocampal-dependent spatial memory and histoarchitectural integrities of the CA regions of Wistar rats following administration of Rauwolfia vomitoria and chlorpromazine
    (Neuroscience Society of Nigeria, 2015) Adana, M. Y.; Imam, A.; Ajibola, M. I.; Abdulmumin, I.; Amin, A. B.; Ibrahim, A.; Olawepo, A.; Imam, A. W.
    Psychotic patients demonstrate poor spatial memory, ascribed to impaired hippocampal functions, and bodies of evidences have attributed cognitive impairments to the poor functional outcomes in psychosis management. The efficacy of chlorpromazine and Rauwolfia vomitoria on spatial memory performance and differential histoarchitecture of the hippocampi of adult Wistar rats was examined in this study. Twenty five adult male Wistar rats weighing between 200 - 230 g were randomly grouped to five (Nor mal, low and high dose chlorpromazine and low and high dose R. vomitoria) of five animals each. 2 ml of normal saline was given to Control animals daily, 5mg/kg of chlorpromazine was given as low dose, 10 mg/kg of chlorpromazine was given as moderate dose, 150 mg/kg of R. vomitoria was given as low dose and 300 mg/kg of R. vomitoria was given as high dose orally. All the medications were given daily for 21 days. A Y-maze apparatus was used to assess the spatial memory performance in the rats at days 14 and 21 of the experiment. All the animals were euthanized using 20 mg/kg of intramuscular ketamine, cardially perfused with 4% paraformaldehyde, the brains and the hippocampus removed for histological analysis. Results from this study show that Rauwolfia at 150 and 300 mg/kg improved the correct decision (right triplet alternation) and reduced wrong decision (wrong triplet alternation) in the treated rats at days 14 and 21 respectively with an unaltered hippocampal histoarchitecture. While chlorpromazine at 5 and 10 mg/kg induced an increased wrong decision (wrong triplet alternation) and reduced correct decision (right triplet alternation) across treatment periods and caused an apparent dis tortion in the hippocampus. In conclusion, R. vomitoria could be a better alternative agent with more therapeutic potential in the treatment of psychosis and could possibly remediate cognitive impairments in psychosis.
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    Histopathological and biochemical evaluation of the antidotal efficacy of Nigella sativa oil on organophosphate-induced hepatotoxicity
    (College of Health Sciences, Osun State University, 2017) Adana, M. Y.; Ajao, M. S.; Abdussalam, W. A.; Imam, A.; Amin, A. B.; Ibrahim, A.; Sulaimon, F. A.; Atata, J. A.
    Objective: The study was designed to investigate the effects of continuous exposure of dichlorvos (DDVP) on hepatic function and hepatic histomorphology, with the possible antidotal efficacy of Nigella sativa oil (NSO). Methods: Twenty four Wistar rats were randomly divided into four groups, with each group comprising of six rats. The groups were labelled as Sunflower oil (SFO), DDVP, DDVP+NSO and NSO. After 14 days of treatments, blood samples were collected, centrifuged and levels of ALP (Alkaline phosphatase), ALT (Alanine aminotransferase), AST (Aspartate aminotransferase) and GGT (γ-glutamyl-transferase) concentrations were estimated in the serum. The livers were removed and prepared for histopathological examinations and evaluation. Results: The findings of the study shows significant increase in the serum concentration of ALT, ALP, AST and GGT with a marked distortion in the hepatic architecture in rats administered with DDVP. However, Nigella sativa oil (NSO) was observed to ameliorate the levels of impairment in the assessed hepatic function parameters and relatively restoration in the hepatic architecture in DDVP+NSO treated animals when compared to the control and group administered with DDVP only. Conclusion: The study concludes that impaired liver functions and histomorphological tissue distortions observed in the experimental rats following DDVP exposure were ameliorated following the administration of NSO.
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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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    Impaired cognitive performance and metabolic disturbance in streptozotocin-nicotinamide induced type 2 diabetes mellitus and the protective effect of Nigerian propolis
    (Nigerian Journal of Neuroscience, 2016) Amin, A.; Saliu, H.; Solomon, E.O.; Sheu, T.; Imam, A.; Abdulmajeed, W.I.; Alli-Oluwafuyi, A.; Ibrahim, R.B.; Owoyele, B.V.
    Defects in insulin signaling and oxidative stress are implicated in cognitive dysfunction in diabetes. This study evaluated the effects of propolis on cognitive impairment in streptozotocin-nicotinamide model of type 2 diabetes mellitus in Wistar rats. Diabetes was induced by single intraperitonieal administration of streptozotocin (65 mg/kg) 15 min after nicotinamide (110 mg/kg) had been adminstered. Diabetic animals were treated with glibenclamide (5 mg/kg), propolis (200 and 300 mg/kg), or normal saline for 4 weeks after which spatial memory was assessed with the Morris’ water maze (MWM). At the end of the study the animals were euthanized and blood collected via cardiac puncture while the brain was homogenized. Insulin was assayed from plasma while malondialdehyde (MDA), superoxide dismutase (SOD), gluthatione (GSH) and catalase were assayed from brain homogenate. Homeostatic model assessment (HOMA) was used as marker for insulin resistance. Significant rise in blood glucose, plasma insulin, and brain MDA (P < 0.05) with reduction in SOD, GSH, and catalase levels were observed in the diabetic group. Treatment with 200 and 300 mg/kg propolis and glibenclamide significantly decreased blood glucose, plasma insulin, and MDA (P < 0.05) and increased brain levels of SOD, GSH and catalase. Propolis (200 and 300 mg/kg) also significantly (P < 0.05) decreased escape latency in the MWM in comparison to the diabetic group. Nigerian propolis thus seems to protect against impaired cognitive performance in experimental diabetes mellitus.
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    Muscle Tissues: In Histology Practical Manual
    (Department of Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, University of Ilorin., 2024-04) Lewu, F. S.; Ibiyeye, R. Y.; Danwahab, O. A.; Imam, A.; Jaji-Sulaimon, R.; Sulaimon, F. A.; Ajao, M. S.; Omotoso. G. O.
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    Nigella sativa Attenuates Trimethyltin-induced Histopathological Changes in Mice Hippocampi
    (National Association of Specialist Medical Doctors in Academics in Nigeria, 2022) Adana M.Y.; Imam, A.; Kareem, S. B.; Ajao, M. S.
    Background: The organotins particularly Trimethyltin (TMT) are very popular in agriculture and industry. Exposure to the compound is associated with several neurological symptoms which suggest neurotoxicity. The study was designed to investigate the antidotal effects of Nigella sativa (NS) on TMT-induced neurotoxicity on mice hippocampi. Materials and Methods: Seventy adult male mice weighing an average of 25g were randomly assigned into seven groups of ten animals each (Groups A- G). Animals in group A were administered single dose TMT (3mg/kg) and euthanized after 48 hours. Groups B, C, and D were given a single dose of TMT (3mg/kg), followed by a single weekly dose of NS (28ml/kg) for 1, 2, and 3 weeks respectively. Groups E, F, and G served as controls for trimethyltin (3mg/kg), Nigella sativa (28ml/kg), and saline (28ml/kg) respectively. NS Results: The mice demonstrated tremors, aggressiveness and subtle seizures at the initial state in TMT administered groups with exophthalmos and pedal edema that subsides in the mice administered with TMT-NS. There were exudes of neuritic plaques, neurofibrillary tangles, and apoptotic cells on TMT-administered brains on histology. These observations were markedly reduced in the TMT-NS administered groups. Conclusion: The study concludes that the neurodestructive effects of TMT on the hippocampal neurons and its ability to negatively affect the neurobehavioral attitudes of the mice could be reversible following the administration of NS
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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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    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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    Oral thymoquinone modulates cyclophosphamide‐induced testicular toxicity in adolescent Wistar rats
    (Wiley, 2022) Adana, M. Y.; Imam, A.; Bello, A. A.; Sunmonu, O. E.; Alege, E. P.; Onigbolabi, O. G.; Ajao, M. S.
    Cyclophosphamide (CYP) is an effective anti-cancer drug that is widely accepted, but it is not devoid of unintended toxic effects. Gonadal toxicity is reported as one of the side effects of its long-time use. This study examined the effects of thymoqui none (TQ) on the biological integrities of the testes after cyclophosphamide expo sure. Thirty adolescent male Wistar rats (100–110 g) were divided into six groups (n = 5), receiving normal saline (NS), 20 mg/kg of CYP (CYP), 5 mg/kg of TQ (TQ5), 10 mg/kg of TQ (TQ10), 20 mg/kg of CYP and 5 mg/kg of TQ (CTQ5), and 20 mg/ kg of CYP and 10 mg/kg of TQ (CTQ10) respectively. On the 22nd day, blood, semen and testicular samples were collected for the assay of serum reproductive hormones (follicle-stimulating (FSH) and luteinizing (LH) hormones), semen analysis and testicu lar histology and proliferating cell nuclear antigen (PCNA) expression. The results re vealed that CYP exposure affected functional and structural integrities of the testes, by depleting sperm count and motility, testosterone, LH, spermatogenic and mature sperm cell population, Leydig cells and PCNA immunoreactive proliferating cells. TQ interventions were able to reverse all cytotoxic CYP impacts, but with differential activities on the hormonal concentrations, specifically LH and FSH. Cumulatively, thymoquinone may be a potent agent against cyclophosphamide effects on the physi ological, regeneration and histological integrities of the testes, as observed in this study.
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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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    Phoenix dactylifera polyphenols ameliorates monosodium glutamate induced cell damage in the dentate gyrus
    (Krishna Institute of Medical Sciences, 2021) Usman, R. Y.; Sulaimon, F. A.; Okesina, A. A.; Imam, A.; Imam, A. L.; Ajao M. S
    Background: Monosodium Glutamate (MSG) use is quite alarming considering the cascades of toxicity that arises from it. However, this study demonstrated the possible ameliorative activities of polyphenols of Phoenix dactylifera (PPD) on MSG-induced dentate gyrus degeneration in male adult Wistar rats. Aim and Objectives: To check the effects of PPD on MSG induced dentate gyrus neuronal damage in adult male Wistar rats. Material and Methods: Groups A to D of adult male rats underwent 14-day treatment of Normal Saline (NS), 500 mg ̸ kg PPD, 4 mg ̸g of MSG only, and 4 mg̸g MSG and 500 mg/kg PPD (MSG+PPD) concurrently. Group E received 500 mg ̸ kg PPD for a 14-day period prior to another 14-day of 4mg ̸ gMSG (PPD then MSG). Results: PPD was able to ameliorate the toxic effect of MSG as evidence of better cellular integrity, minimal cell vacuolations, minimized dispersed Nissl bodies and deeply stained Nissl bodies were observed upon PPD administration. It was also observed that it reduced the proliferation of reactive oxygen species, proteins and DNAdamage in the cells of the dentate gyrus. Conclusion: The study concluded that PPD was able to ameliorate the degeneration induced by MSG in the dentate gyrus of Wistar rats
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    Subchronic dichlorvos-induced Cardiotoxicity in Wistar rats: Mitigative efficacy of Nigella sativa oil.
    (2018) Adana, M. Y.; Imam, A.; Busari, M. O.; Ajibola, M. I.; Ibrahim, A.; Sulaimon, F. A.; Ajao, M. S.
    BACKGROUND: Accidental poisoning from indiscriminate use of organophosphates have become endemic in recent decades, most especially in developing nations, coupled with the limitations of the availability of satisfactory antidotes. AIM OF THE STUDY: Thus, we investigated the cardioprotective efficacy of Nigella sativa oil (NSO) following dichlorvos dichlorvos (DDVP)‑induced cardiotoxicity in Wistar rats. MATERIALS AND METHODS: A total of 24 Wistar rats were randomly divided into four groups (n = 6); the control was administered sunflower oil (1 ml/kg), DDVP (8.8 mg/kg) to the experimental Group I, whereas DDVP + NSO (8.8 mg/kg +1 ml/kg) and NSO (1 ml/kg) was administered orally to the experimental Groups II and III, respectively. The animals were euthanized; blood was transcardially collected from the right atrium, centrifuged, and plasma extracted to analyze levels of total cholesterol (TC), triglycerides, high‑density lipoprotein cholesterol, and low‑density lipoprotein cholesterol (LDL‑C). While cardiac muscle tissue was collected from the left heart, processed and stained for general architecture (hematoxylin and eosin) and elastic morphology (orcein). RESULTS: DDVP significantly (P ≤ 0.05) increased the plasma levels of TC, LDL, atherogenic and atherosclerotic indices (TC/HDL‑C and LDL‑C/HDL‑C ratios), but this was prevented by co-administration with NSO. Histological investigations showed that DDVP resulted in the pathological appearance of cardiac tissues, such as the lack of striations, myocardial hemorrhage, and necrosis‑like features. CONCLUSION: It can be concluded that NSO was able to attenuate DDVP‑induced cardiotoxicity.
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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.
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    Thymoquinone Ingestions Reversed Inflammation Driven Glia activation and Impaired Cognitive associated behavior in Cypermethrin Exposed Rats.
    (Uskudar University, 2024) Imam, A. L.; Okesina, A. A.; Sulaimon, F. A.; Imam, A.; Ibiyeye, R. Y.; Adana, M. Y.; Omoola, O. O.; Ajao, M. S.
    Background: Pyrethroids pose health risks to humans. Therefore, it is imperative to assess the preventive benefits of thymoquinone against neurotoxicity induced by cypermethrin- in the hippocampal dentate gyrus. Methods: Forty male adult Wistar rats with an average weight of 180-200g were randomly allocated to five (5) groups, and each comprising eight rats (n=8 per group). The groups were designated as follows, through oral administrations for 14 days: 0.5ml phosphate- buffered saline (PBS) was given to group one; Group two received 20mg/kg of cypermethrin (CYM); Group three received 10 mg/kg of thymoquinone (THQ); Group four received 20 mg/kg of cypermethrin followed by 10mg/kg of thymoquinone (CYM-10mgTHQ); and Group five received 20mg/kg and 5mg/kg cypermethrin and thymoquinone respectively (CYM-5mgTHQ). Behavioral, histological, immunohistochemical, and biochemical analyses were conducted post-treatment. Results: Cypermethrin administration caused the rise in pro-inflammatory cytokine TNF-α and increased expression of astrocytes, microglia, and pro-apoptotic protein Bax. Additionally, cypermethrin reduced levels of anti-inflammatory cytokine IL-10, acetylcholinesterase (AChE) activity, and nuclear factor erythroid 2-related factor 2 (Nrf2). cytoarchitectural disruption of dentate gyrus and decreased Nrf2 expression were observed. Cognitive deficits were evident. Thymoquinone treatment attenuated TNF-α elevation, reduced astrocyte, microglial, and Bax expression, and increased IL-10, AChE, and Nrf2 levels. Conclusion: Thymoquinone demonstrated anti-inflammatory and anti-apoptotic effects against cypermethrin-induced neurotoxicity, improving cognitive function in rats.