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CC BY-NC-ND 4.0 · Libyan International Medical University Journal 2020; 05(02): 37-47
DOI: 10.4103/LIUJ.LIUJ_29_20
Original Article

Doxycycline: An antibiotic with brain protective function in vanadium-intoxicated rats

Negia Emtawel Mohamed
Department of Biochemistry, Faculty of Medicine, Benghazi University, Benghazi, Libya
,
Ezeddin Gassar
1   Department of Physiology, Faculty of Medicine, Benghazi University, Benghazi, Libya
,
Sara Abdulla
Department of Biochemistry, Faculty of Medicine, Benghazi University, Benghazi, Libya
,
Mustafa Elfakhri
Department of Biochemistry, Faculty of Medicine, Benghazi University, Benghazi, Libya
,
Ayyub Patel
1   Department of Physiology, Faculty of Medicine, Benghazi University, Benghazi, Libya
,
Syed Haider
2   Department of Clinical Biochemistry, College of Medicine, King Khalid University, Abha, Saudi Arabia
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Abstract

Background: Exposure to vanadium exhibits deleterious neurotoxicity. Doxycycline is a potential antioxidant that prevents the progression of disease through inhibition of lipid peroxidation. Objectives: This research investigates the neuroprotective effects of doxycycline, in different rat brain areas in an animal model intoxicated with vanadium. Materials and Methods: Male Sprague-Dawley rats were equally divided into the following four groups: control group, doxycycline-treated group, vanadium-treated group, and concomitant doses of doxycycline plus vanadium-treated group, all given orally for 10 consecutive days. The animals were watched daily for any signs of neurological defects. They were sacrificed by decapitation 24 h after the last dose. Brain was removed rapidly and dissected into cerebral cortex, cerebellum, and brain stem. Biochemical studies including the concentrations of phospholipids, cholesterol, cerebrosides, glutathione (GSH), acetylcholinesterase (AChE) activity, gangliosides, ascorbic acid, calcium, and lipid peroxidation levels were determined. Results: The results revealed that vanadium produced significant reduction in body and absolute brain weight, with neurological function deficits. Vanadium significantly decreased the concentrations of phospholipids, cholesterol, cerebrosides, and GSH and inhibited AChE activity together with significant increase in gangliosides, ascorbic acid, calcium, and lipid peroxidation levels compared to saline controls. Animals which were given the combined treatment of vanadium and doxycycline regained weight and became normal. Moreover, doxycycline reversed the effect of vanadium on the metabolic variables and inhibited lipid peroxidation nearing to normal levels to that of saline controls. Conclusion: These findings demonstrated the antioxidant or chelating action of doxycycline against vanadium neurotoxicity and its therapeutic potential to avert neurodegenerative changes in different rat brain areas.

Key-words:

Doxycycline - lipid peroxidation - neuronal deficits - neurotoxicity - reactive oxygen species - vanadium

Financial support and sponsorship

Nil.




Publication History

Received: 05 July 2020

Accepted: 24 July 2020

Article published online:
14 June 2022

© 2020. Libyan International Medical University. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

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