Institute of Development Studies Publications

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Institute of Development Studies Publications

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Browsing Institute of Development Studies Publications by Author "Abdussalam, B."

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    Nigella sativa oil attenuates aluminum-induced behavioral changes, oxidative stress and cortico-hippocampal neuronal degeneration in rats
    (2020-07) AbdulAzeez, T.O.; Aminu, I.; Abdussalam, B.; Samson, C.; Abdul-musawwir, A.; Asma’u, S.M.; Rukayat, J.; Shittu, S.T.; Abdulmumin, I.; Salihu, A.M.
    Aluminum (AlCl3) usage in both the industrial and domestic arena has dramatically risen over time owing to its ubiquity and utility for many activities despite frequent reporting of its neurotoxic effects over wide range of concentrations. The neuro-protective effects of Nigella sativa Oil (NSO) following intermediate exposure to aluminum salts has largely been unexplored. The present study explores the ameliorative and neuro-protective functions of NSO on aluminum chloride (AlCl3)-induced damages in the frontal cortices and hippocampus of exposed rats. Methods: The study involved the use of thirty two adult male Wistar rats weighing 180 ± 20 g, randomly divided into four groups, in which group 1 received saline, group 2 received AlCl3 (100 mg/kg), group 3 received AlCl3 (100 mg/kg) followed by NSO (1 ml/kg) 30 min later, while group 4 received NSO (1 ml/kg) only. All administrations were done orally for 14 days. Standardized behavioural tests for anxiety and cognitive performance were carried on after the treatments prior to euthanizing (Ketamine 10 mg/kg, ip). On day 15, the rats were euthanized, and their brains excised, with the frontal cortex and hippocampus removed. Five of these samples were homogenized and centrifuged to analyze nitric oxide (NO) metabolites and total reactive oxygen species (ROS), and the other three were processed for histology (cresyl violet stain) and proliferative markers (Ki67 immunohistochemistry). Results: Increased Transfer latency, time in dark box, escape latency and reduced rearing frequency, percentage alternation and time in platform quadrant were observed in the AlCl3 exposed rats. There was also an increased level of ROS and NO in the brain regions with marked inhibition of neuronal cell proliferation as evidenced by reduced Ki-67 protein expression in the brain of AlCl3 only rats. However, rats co-administered AlCl3 and NSO showed significantly reduced ROS and NO levels, improved anxiety-like and cognitive behaviors and increased Ki-67 expression when compared with AlCl3 only treated rats. Conclusion: AlCl3 exposure causes neuronal damage and impaired anxiety-like and memory indices which are associated with increased free radical generation and inhibited neuronal proliferation, whereas the antioxidant and neuro-protective properties of NSO were efficacious against the observed effects