Browsing by Author "Kadir, R. E."

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    Altered testicular histomorphometric and antioxidant levels following in vivo bisphenol-a administration
    (Arak University of Medical Sciences, 2021) Kadir, R. E.; Ojulari, S. L.; Gegele, A. T.; Lawal, A. I.; Sulu-Gambari, L.; Sulaimon, F. A.; Omotoso, G. O.
    Background: Bisphenol-A (BPA) is a pervasive environmental toxin that is used in the production processes of many consumables and equipment that are in daily application. The aim of this study was to determine the effects of BPA on the structural and functional integrity of the reproductive system in male Wistar rats and its interaction with melatonin. Methods: Adult female rats in pro-estrus phases were mated with adult male rats and the conception determined. The male pups were divided into two groups of A and B. These groups were further subdivided into six subgroups each. They were administered varying low doses of BPA (25 or 50mg/kg) and melatonin (10mg/kg) at neonatal and adolescent ages. The testes, epididymis and blood samples were collected for histological, semen and biochemical investigations, respectively. Results: The results show that BPA caused histological alterations, reduced quality and quantity of sperm cells, and induced oxidative stress at birth and adolescence. Conclusion:Bisphenol A exposure, even at low dose, is toxic to the male reproductive system, and melatonin administration did not significantly improve the alterations caused by the BPA.
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    Anticancer effects of Morinda lucida and Annona muricata on immunomodulations of Melatonin, tumor necrosis factor-alpha and p53 concentrations in lead acetate-induced toxicity in rats
    (Qassim University, 2021-07) Akinlolu, A. A.; Ameen, M. O.; Oyewopo, A. O.; Kadir, R. E.; Ahialaka, O.; Tijani, S.; Ogungbesan, O.; Bebeyi, R.; Adebayo, S.; Amoo, T.; Abdulazeez, M.
    Objectives: Lead poisoning accounts for about 0.6% of global burden of disease. Lead-induced toxicity is through confinement of oxidative stress in affected organs. We evaluated the effects of MLF1 (extracted from Morinda lucida leaves) and AMF1 (extracted from Annona muricata leaves) on lipid peroxidation and immunomodulations of Melatonin, tumor necrosis factor-alpha (TNF-α), and p53 proteins in lead acetate (LA)-induced toxicity in rats. Methods: Sixty adult female rats were randomly divided into 12 groups (n = 5). Groups 1 and 2 received physiological saline and 100 mg/kg bodyweight of LA, respectively, for 5 weeks. Groups 3–6 received 100 mg/kg bodyweight LA for 2 weeks, followed by treatments with 7.5 and 15 mg/kg bodyweight of MLF1, and 7.5 and 10 mg/kg bodyweight of AMF1, respectively, for 3 weeks. Groups 7–10 received 7.5 and 15 mg/kg bodyweight of MLF1, 7.5 and 10 mg/kg bodyweight of AMF1, respectively, for 5 weeks. Groups 11–12 received co-administrations of 100 mg/kg bodyweight LA with 15 mg/kg bodyweight MLF1 and 10 mg/kg bodyweight of AMF1, respectively, for 5 weeks. Drugs and extracts were administered orally. Consequently, liver histopathology (Hematoxylin and Eosin), sera Melatonin, and TNF-α (enzyme-linked immunosorbent assay [ELISA]) levels were evaluated. Malondialdehyde (MDA) (thiobarbituric acid assay) and p53 (ELISA) levels were evaluated in liver homogenates. Data were statistically analyzed (P ≤ 0.05). Results: Results showed normal liver histology in all Groups. Statistical analyses showed significant (P ≤ 0.05) and non-significant decreased levels (P ≥ 0.05) of MDA, TNF-α and p53 in Groups 3-12, compared with Group 2. Furthermore, results showed significant (P ≤ 0.05) and non-significant increased Melatonin levels (P ≥ 0.05) in Groups 4–12 compared with Group 2. Conclusion: This study confirmed that MLF1 and AMF1 confer a degree of antioxidant, anticancer and hepato-protetive potentials against LA-induced toxicity in rats.
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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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    Moringa oleifera Ameliorates Cuprizone-Induced Cerebellar Damage in Adult Female Rats
    (https://www.ajol.info/index.php/rejhs/issue/view/16912, 2018) Omotoso, G. O.; Kadir, R. E.; Lewu, S. F.; Gbadamosi, I, T.; Akinlolu, A. A.; Adunmo, G. O.; Kola, R. M.; Lawal, M. O.; Ameen, M. O.
    Objectives: Cuprizone is a neurotoxicant used in modeling demyelinating disorders. This study explored the effects of Moringa oleifera (MO) on oxidative, histomorphological and behavioural changes in cuprizone-damaged cerebellum. Methods: Twenty adult female Wistar rats were grouped into 4, each group having five animals. Group A received 1 ml of normal saline (Control); group B received 0.4% cuprizone; group C received 15.6 mg/kgBW Moringa oleifera leaf extract; group D received 0.4% cuprizone and 15.6 mg/kgBW Moringa oleifera, orally for 5 weeks. The animals were assessed for exploratory and locomotor activities, while the cerebellum was processed for histology and assayed for nitric oxide (NO), catalase (CAT) and superoxide dismutase (SOD) activities. Results: Cuprizone treatment caused weight reduction, disruption of Purkinje cell layer, cellular degeneration, reduction in NO, CAT and SOD activities. However, these changes were ameliorated when co-administered with MO. Conclusion: The anti-oxidative property of Moringa oleifera is responsible for its ameliorative effect in cuprizone neurotoxicity.
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    Moringa oleifera and Musa sapientum ameliorated 7,12-Dimethylbenz[a]anthracene-induced upregulations of Ki67 and multidrug resistance 1 genes in rats
    (Qassim University, 2021-05) Akinlolu, A. A.; Oyewopo, A. O.; Kadir, R. E.; Lawal, A.; Ademiloye, J.; Jubril, A.; Ameen, M. O.; Ebito, G. E.
    Objectives: Moringa oleifera (MO) and Musa sapientum (MS) are plants of ethnomedicinal importance. We evaluated the effects of MOF6 (extracted from MO leaves) and MSF1 (extracted from MS suckers) on immunomodulations of Ki67 (proliferation biomarker) and multidrug resistance 1 (MDR1) genes in the liver of rats in 7,12-Dimethylbenz[a]anthracene (DMBA)-induced hepatotoxicity and mutagenesis to determine their antiproliferation, anti-drug resistance, and anticancer potentials. Methods: Forty-five adult male rats were randomly divided into nine groups (n = 5). Groups 1 and 2 received physiological saline and 15 mg/kg bodyweight of DMBA, respectively. Groups 3 and 4 received 15 mg/kg bodyweight DMBA and were treated with 15 and 30 mg/kg bodyweight of MOF6, respectively. Group 5 received 15 mg/kg bodyweight DMBA and was treated with 10 mg/kg bodyweight of MSF1. Group 6 received 15 mg/kg bodyweight DMBA and was treated with 3.35 mg/kg bodyweight of doxorubicin and intravenous injection of 0.5 ml/200 g of cisplatin. Groups 7–9 received only 15 and 30 mg/kg bodyweight of MOF6 and 10 mg/kg bodyweight of MSF1, respectively. DMBA, doxorubicin, and extracts doses were administered orally. The duration of our experimental procedure was 8 weeks. Consequently, liver histopathology (hematoxylin and eosin technique) and enzyme-linked immunosorbent assay homogenates’ concentrations of Ki67 and MDR1 were evaluated. Computed data were statistically analyzed (P ≤ 0.05). Results: Results showed normal histoarchitectures of the liver in all groups. Statistical analyses showed significant (P ≤ 0.05) and non-significant decreased concentrations (P ≥ 0.05) of Ki67 and MDR1 in Groups 3–9 compared with Group 2. Therefore, MOF6 and MSF1 ameliorated DMBA-induced hepatotoxicity, abnormal proliferation, and drug resistance. Conclusion: MOF6 and MSF1 possess antiproliferation, anti-drug resistance, and anticancer potentials.
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    Moringa oleifera IS PROTECTIVE AGAINST MICROARCHITECTURAL AND NEUROCHEMICAL CHANGES ASSOCIATED WITH CUPRIZONEINDUCED PREFRONTAL CORTEX NEUROTOXICITY IN FEMALE WISTAR RATS
    (Neuroscience Society of Nigeria (NSN), 2018-05-20) Omotoso, G. O.; Gbadamosi, I. T.; Akinlolu, A, A.; Ameen, Mubarak; Kadir, R. E.; Jaji-Sulaimon, R.; Abdulwahab, A. B.; Kolo, R. M.
    Cuprizone administration causes selective damage to axonal myelin sheath and has been used to model demyelinating diseases in neuroscience research. This study aimed at determining the protective effects of Moringa oleifera on cuprizone-induced neurotoxicity in the prefrontal cortex (PFC). Sixteen adult female Wistar rats were procured and grouped into 4: Group A was given normal saline, Group B received 0.4% cuprizone diet, Group C was administered with 1.875 mg/ml of Moringa oleifera and Group D received a combination of 0.4% cuprizone diet and 1.875 mg/ml of Moringa oleifera. All the groups were treated orally for 35 consecutive days after which they were sacrificed. Thereafter the PFC was processed for histological demonstration, while tissue homogenate was used to assay the activity of superoxide dismutase (SOD). Cuprizone administration caused significant reduction in body weight and SOD activities. It also caused an alteration in the microarchitecture and Nissl profile of the PFC. Moringa oleifera intervention led to restoration of body weight, SOD levels, Nissl profile and the histology of the PFC. The use of preparations of Moringa oleifera, especially the leaf-component, could offer some protective measures to individuals suffering from demyelinating conditions, especially in addressing the associated weight changes and frontocortical dysfunction.
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    Research Journal of Health Sciences
    (2018-02-01) Omotoso, G. O.; Kadir, R. E.; Gbadamosi, I. T.; Akinlolu, A. A.; Adunmo, G. O.; Kolo, R. M.; Lawal, M. O.; Ameen, M. O.
    Objectives: Cuprizone is a neurotoxicant used in modeling demyelinating disorders. This study explored the effects of Moringa oleifera (MO) on oxidative, histomorphological and behavioural changes in cuprizone-damaged cerebellum. Methods: Twenty adult female Wistar rats were grouped into 4, each group having five animals. Group A received 1 ml of normal saline (Control); group B received 0.4% cuprizone; group C received 15.6 mg/kgBW Moringa oleifera leaf extract; group D received 0.4% cuprizone and 15.6 mg/kgBW Moringa oleifera, orally for 5 weeks. The animals were assessed for exploratory and locomotor activities, while the cerebellum was processed for histology and assayed for nitric oxide (NO), catalase (CAT) and superoxide dismutase (SOD) activities. Results: Cuprizone treatment caused weight reduction, disruption of Purkinje cell layer, cellular degeneration, reduction in NO, CAT and SOD activities. However, these changes were ameliorated when co-administered with MO. Conclusion: The anti-oxidative property of Moringa oleifera is responsible for its ameliorative effect in cuprizone neurotoxicity.