Nigella sativa oil protected the hippocampus against Acetyl cholinesterase and oxidative dysfunctions-driven impaired working memory in rats

Document Type : Original Article

Authors

1 Neuroscience Unit, Department of Anatomy, College of Health Sciences, University of Ilorin, Nigeria.

2 Comparative Neurobiology Unit, School of Anatomical sciences, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, Republic of South Africa.

3 Neurophysiology Unit, Department of Physiology, College of Health Sciences, University of Ilorin, Nigeria.

4 Department of Oral science, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, Republic of South Africa.

5 Endocrinology and metabolism Research Unit, Department of Physiology, College of Medicine, University of Ibadan, Ibadan, Nigeria.

Abstract

Oxidative damages in organophosphates poisoning is associated with neuro-cognitive deficits. This study investigates the protective effect of Nigella sativa oil (NSO) in mitigating dichlorvos (DDVP) induced oxidative damage and neuro-cognitive impairment in rats. Thirty-two rats were randomly divided into four groups, exposed to 1 ml/kg of normal saline, 8.8 mg/kg of DDVP, DDVP + 1 ml/kg of NSO and NSO respectively for 14 consecutive days. Body weights were recorded at day 1 and 15 of the experiment, the rats were exposed to 3 trials each on the 11, 12 and 13th days in the Morris water maze, and subsequently latency to hidden platform and time in the platform quadrant were recorded as measures of long term memory (LTM), short term memory (STM) and reference memory on the 14th day. The rats were euthanized on the 15th day, the brains excised and the hippocampi of five brains in each group were removed, homogenized to analyze for total reactive oxygen species (ROS), nitrous oxide (NO) levels and acetylcholinesterase (AChE) activities, while the other three were processed for histology and Ki67 immunohistochemistry. DDVP exposure caused a significant increase in hippocampal NO and ROS levels, with reductions in AChE activities and Ki67 protein expression. This was associated with delayed escape latency and reduced time in platform quadrant. NSO intervention prevented outburst in ROS and NO, preserved the neurogenic cells and improved neuro-cognitive indices. We thus conclude that stabilizing oxidative and neurogenic functions are vital to protect against DDVP hippocampal insults.

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