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Anat Cell Biol

Published online August 25, 2020

https://doi.org/10.5115/acb.20.099

Copyright © Korean Association of ANATOMISTS.

Inhibitory potentials of Cymbopogon citratus oil against aluminium-induced behavioral deficits and neuropathology in rats

Gbadamosi Ismail Temitayo1 , Bamisi Olawande1 , Yawson Olushola Emmanuel1,2 , Arogundade Tolulope Timothy1,2 , Ogunrinola Kehinde1 , Lewu Folashade Susan1 , Lambe Ezra1 , Olajide Olayemi Joseph1,3

1Division of Neurobiology, Department of Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, University of Ilorin, Ilorin, 2Division of Neurobiology, Department of Anatomy, Faculty of Basic Medical Sciences, Adeleke University, Ede, Nigeria, 3Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University Montreal, Montreal, Quebec, Canada

Correspondence to:Gbadamosi Ismail Temitayo
Division of Neurobiology, Department of Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, University of Ilorin, Ilorin, PMB 1515, Nigeria
E-mail: ismail.tayo@yahoo.com

Received: April 23, 2020; Revised: May 19, 2020; Accepted: May 25, 2020

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Cymbopogon citratus is a tropical phytomedicinal plant that is widely known for its hypoglycemic, hypolipidemic, anxiolytic, sedative, antioxidative and anti-inflammatory properties. In this study, we have examined the neuroprotective effects of the essential oil (ESO) of Cymbopogon citratus, following aluminum chloride (AlCl3)-induced neurotoxicity within the cerebellum of Wistar rats. A total of 40 adult male Wistar rats were assigned into five groups and treated orally as follows: A–phosphate-buffered saline (1 ml daily for 15 days); B–ESO (50 mg/kg daily for 15 days); C–AlCl3 (100 mg/kg daily for 15 days); D–AlCl3 then ESO (100 mg/kg AlCl3 daily for 15 days followed by 50 mg/kg ESO daily for subsequent 15 days); E–ESO then AlCl3 (50 mg/kg ESO daily for 15 days followed by 100 mg/kg AlCl3 daily for following 15 days). To address our questions, we observed the locomotion and exploratory behavior of the rats in the open field apparatus and subsequently evaluated cerebellar oxidative redox parameters, neural bioenergetics, acetylcholinesterase levels, transferrin receptor protein, and total protein profiles by biochemical assays. Furthermore, we investigated cerebellar histomorphology and Nissl profile by H&E and Cresyl violet Nissl staining procedures. ESO treatment markedly attenuated deficits in exploratory activities and rearing behavior following AlCl3 toxicity, indicating its anxiolytic potentials. Additionally, AlCl3 evokedincrease in malondialdehyde and nitric oxide levels, as well as repressed cerebellar catalase, glutathione peroxidase, and superoxide dismutase profiles were normalised to baseline levels by ESO treatment. Treatment with ESO, ergo, exhibits substantial neuroprotective and modulatory potentials in response to AlCl3 toxicity.

Keywords: Cerebellum, Cymbopogon, Inflammation, Oxidative stress

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