Cortico-hippocampal molecular characterization in rat model of multiple sclerosis: Neuroprotective mechanisms of Nigella sativa oil Rhoda Mama Kolo, Chijoke Bethel Ehirim, Damilola Opeadua Olabiyi, Isaac Ayobami Ayobamidele, Rukayat Jaji-Sulaimon, et al. Multiple Sclerosis Journal Experimental Translational and Clinical, 2025 Background Current multiple sclerosis management primarily targets symptom alleviation and immune modulation, with limited success in halting progression or achieving sustained remission. Consequently, the development of novel therapeutic strategies targeting the underlying mechanisms of multiple sclerosis (MS) remains a critical area of research. Objectives This study investigated the putative neuroprotective properties of Nigella sativa oil (NSO) in a cuprizone-induced demyelination model in adult male Wistar rats. Methods Twenty-four adult male Wistar rats were divided into four groups: Group A (Control) received normal mash feed; Group B received 0.2% cuprizone diet; Group C received 5 ml/kg NSO, while Group D received 0.2% cuprizone diet and 5 ml/kg NSO. After 35 days, rats were tested for memory and behaviour (Y-maze, Morris water maze, open-field test). Rats were euthanized, brains were excised then examined for myelin integrity, oligodendrocyte loss, and microglial activation using immunohistochemistry (antibodies: myelin basic protein, oligodendrocyte transcription factor, ionized calcium-binding adaptor molecule 1). Results Cuprizone exposure resulted in impaired memory function, reduced exploratory behaviour, and increased anxiety-like behaviours. Treatment with NSO mitigated these behavioural deficits. Additionally, NSO treatment reduced microglial activation and preserved myelin integrity. Conclusion Nigella sativa oil ameliorated behavioural alterations, neuroinflammation and demyelination in cuprizone model of MS, suggesting that NSO may have therapeutic potential for MS.
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 Fatimo Ajoke Sulaimon, Ruqayyah Yetunde Ibiyeye, Aminu Imam, Aboyeji Lukuman Oyewole, Abubakar Lekan Imam, et al. Anatomy and Cell Biology, 2024 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.
Calcium Supplementation Ameliorates Cerebellar Oxidative Stress in Lactational Aluminum-induced Neurotoxicity in Rats Gabriel Olaiya Omotoso, Ridwan Adeniyi Olanrewaju, Nathaniel O. Amedu, Rhoda Mama Kolo, Ismail Temitayo Gbadamosi, et al. Basic and Clinical Neuroscience, 2022 Introduction: The neurotoxic effects of aluminum exposure during the critical period of neurodevelopment have been well documented. This study investigated the known protective effects of calcium supplementation on the cerebellum of juvenile Wistar rats following aluminum-induced neurotoxicity during lactation. Methods: Four groups of juvenile rats were exposed via lactation to distilled water (control group), aluminum (40 mg/kg/d), calcium supplement (50 mg/kg/d), and a combination of both aluminum and calcium from postnatal day 4 to day 28. The cerebella of the animals were excised to access the levels of antioxidant enzymes (superoxide dismutase [SOD], glutathione peroxidase [GPx]), lipid peroxidation (malondialdehyde), histomorphological alterations (hematoxylin and eosin staining), Nissl profile (cresyl fast violet staining), and glial activation (glial fibrillary acidic protein immunohistochemistry). Results: Lactational aluminum significantly decreased the activities of superoxide dismutase and glutathione peroxidase while exacerbating lipid peroxidation and reactive astrocyte in cerebellar lysates. Lactational calcium supplementation normalized the activities of SOD and GPx, thereby preventing excessive lipid peroxidation and glial activation. Despite no apparent changes in the general histology of the cerebellum, aluminum-induced chromatolysis changes in the Purkinje cell layer, which was counteracted by the antioxidant propensities of calcium supplementation. Conclusion: These findings support that calcium supplementation significantly protects the cerebellum against aluminum-induced oxidative stress, chromatolysis, and neuroinflammation.
Altered testicular histomorphometric and antioxidant levels following in vivo Bisphenol-A administration Eniola Risikat Kadir, Lekan Sheriff Ojulari, Taiye Abdullah Gegele, Ismail Adetayo Lawal, Lukman Sulu-Gambari, et al. Iranian Journal of Toxicology, 2021 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.
Lead acetate-induced neurodegenerative changes in the dorsolateral prefrontal cortex of mice: The role of vitexin Nathaniel Ohiemi Amedu, Gabriel Olaiya Omotoso Environmental Analysis Health and Toxicology, 2020 This study was aimed at investigating the neuroprotective effect of Vitexin against lead (Pb) induced neurodegenerative changes in the dorsolateral prefrontal cortex (DLPFC) and working memory in mice. Thirty-two adolescent male albino mice were divided into four groups (n=8). Control group received 0.2 mL of normal saline; Pb group received 100 mg/kg of Pb acetate for 14 days, Vitexin group received 1mg/kg of Vitexin for 14 days, and Pb+Vitexin group received 100 mg/kg of Pb acetate and 1 mgkg of Vitexin for 14 days. Barnes maze test and novel object recognition test were done to ascertain working memory. Histoarchitectural assessment of DLPFC was done with haematoxylin and eosin (H&E), cresyl fast violet and congo red stains. Furthermore, cell count and other morphometric measurements were done. There was significant decline in working memory in the Pb group, but a combination of Pb+Vitexin improved the working memory. Vitexin significantly reduced neuronal death and chromatolysis caused by Pb. Amyloid aggregation was not observed in any of the groups. This study has shown that concurrent administration of Vitexin and Pb will significantly reduce neurodegeneration and improve working memory. However, Pb treatment or Pb+Vitexin treatment does not have any effect on intercellular distance, neuronal length and the cross-sectional area of neurons in layer III of DLPFC.
Moringa regimen corrects nicotine-induced deficits in behaviour, altered energy metabolism and neurotransmitter processing in Rat Brain Journal of Krishna Institute of Medical Sciences University, 2019
Moringa oleifera ameliorates histomorphological changes associated with cuprizone neurotoxicity in the hippocampal Cornu ammonis (CA) 3 region Nigerian Journal of Physiological Sciences, 2018
Morphological and neurohistological changes in adolescent rats administered with nicotine during intrauterine life Nigerian Journal of Physiological Sciences, 2013
