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Background: Alzheimer's is a complex neurodegenerative disease and is characterized by extraneuronal accumulation of β-amyloid peptide. Because of its complex nature, multi-target directed ligands (MTDLs) are increasingly being considered as promising anti-Alzheimer therapeutic agents. This study is aimed at determining the effects of Cassia tora ethyl acetate fraction on several Alzheimer-associated deleterious events in test tubes as well as in human neuroblastoma SK-N-SH and SH-SY5Y cell lines., Method: Ethyl acetate fraction of C. tora was purified by chromatography, characterized by 1 H and 13 C NMR, and tested for its ability to prevent Aβ 1-42 aggregation by thioflavin-T fluorescence and transmission electron microscopy. We also analyzed the intracellular ROS level and cytotoxicity in SK-N-SH and SH-SY5Y cell lines., Results: The extract inhibits the formation of Aβ 1-42 aggregation from monomers and oligomers, as also acetylcholinesterase activity, Aβ 1-42 -induced cell death, and Aβ 1-42 -dependent intracellular ROS production in both SK-N-SH and SH-SY5Y cells. In-depth chromatographic and spectroscopic analysis of the extract revealed that the active molecules are most likely triglycerides of oleic acid (C 18 H 34 O 2 )., Conclusion: We demonstrate for the first time that Cassia tora fraction prevents Aβ 1-42 aggregation, inhibits acetylcholinesterase and alleviates Aβ 1-42 -induced oxidative stress in human neuroblastoma cells. We further suggest the possible use of triglycerides of oleic acid as efficient anti-Alzheimer agents., (Copyright © 2019. Published by Elsevier B.V.)

Background: Motor dysfunctions are some of the characteristic symptoms of organophosphate (OP) poisoning and they have been associated with decreased levels of cholinesterase inhibition within motor areas of the brain. Objectives: The current study aims to investigate the potential neuroprotective effects of Nigella sativa oil (NSO) in alleviating chlorpyrifos (CPF) induced toxicity in the cerebella and motor cortices of the rat brains using combined behavioural, biochemical and histochemical methods. Methods: Thirty-two rats were randomly divided into four groups (eight rats per group), exposed to 1ml/kg of normal saline, 14.9 mg/kg of CPF, 14.9 mg/kg of CPF plus 1ml/kg of NSO and 1ml/kg of NSO respectively for 14 consecutive days. The rats were each exposed to a single trial of the Open Field Test (OFT) on day 13 of the experiment. This experimental test measured locomotor activity levels (line crossing frequency (LCF)) and exploratory (rearing frequency (RF)) activities in the rats studied. The rats were euthanized on day 15 of the experiment and the brains were subsequently excised. The cerebella cortices of five brains were removed and homogenised to analyse for total reactive oxygen species (ROS), nitric oxide (NO) levels and acetylcholinesterase (AChE) activity. The motor and cerebella cortices from three other brains in each group were processed for histology (Nissl stain) and proliferative activity (Ki67 immunohistochemistry). Results: Rats exposed to CPF experienced a significant increase in cerebella NO and ROS levels, depletion in AChE activity, neurogenic cells loss and subsequent reduction in locomotor and exploratory behaviours respectively (LCF and RF). However, interventional treatment with NSO depleted markers of oxidative damage (NO and ROS), reduced AChE inhibition, preserved neurogenic (Ki67) cells distribution and motor functions. Conclusion: These results demonstrate the potential efficacy of NSO in OP poisoning and the roles of neurogenic and oxidative functions in the pathophysiology and treatment of motor dysfunction in OP neurotoxicity.

Introduction: Motor dysfunctions are some of the characteristic symptoms of organophosphate (OP) poisoning and they have been associated with decreased levels of cholinesterase inhibition within motor areas of the brain. The current study aims to investigate the potential neuroprotective effects of Nigella sativa oil (NSO) in alleviating chlorpyrifos (CPF) induced toxicity in the cerebellar and motor cortices of the rat brains using combined behavioural, biochemical and histochemical methods. Methods and Materials: Thirty-two rats were randomly divided into four groups (eight rats per group), exposed to 1ml/kg of normal saline, 14.9 mg/kg of CPF, 14.9 mg/kg of CPF plus 1ml/kg of NSO and 1ml/kg of NSO respectively for 14 consecutive days. The rats were each exposed to a single trial of the Open Field Test (OFT) on day 13 of the experiment. This experimental test measured locomotor activity levels (line crossing frequency (LCF)) and exploratory (rearing frequency (RF)) activities in the rats studied. The rats were euthanized on day 15 of the experiment and the brains were subsequently excised. The cerebellar cortices of five brains were removed and homogenised to analyse for total reactive oxygen species (ROS), nitric oxide (NO) levels and acetylcholinesterase (AChE) activity. The motor and cerebellar cortices from three other brains in each group were processed for histology (Nissl stain) and proliferative activity (Ki67 immunohistochemistry). Results: Rats exposed to CPF experienced a significant increase in cerebellar NO and ROS levels, depletion in AChE activity, neurogenic cells loss and subsequent reduction in locomotor and exploratory behaviours respectively (LCF and RF). However, interventional treatment with NSO depleted markers of oxidative damage (NO and ROS), reduced AChE inhibition, preserved neurogenic (Ki67) cells distribution and motor functions. Conclusion: These results demonstrate the potential efficacy of NSO in OP poisoning and the roles of neurogenic and oxidative functions in the pathophysiology and treatment of motor dysfunction in OP neurotoxicity. [ABSTRACT FROM AUTHOR]