alexa Ethane-β-Sultam Modifies the Activation of the Innate Immune System Induced by Intermittent Ethanol Administration in Female Adolescent Rats
ISSN: 2329-6488

Journal of Alcoholism & Drug Dependence
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Research Article

Ethane-β-Sultam Modifies the Activation of the Innate Immune System Induced by Intermittent Ethanol Administration in Female Adolescent Rats

Stefanini C1, Colivicchi MA1, Della Corte L1, Ward RJ1,2,4*, De Witte P2, Lallemand F2, Hemmings K3, Pitard A3, Page MI3, Nayak K4 and Dexter DT4

1Dipartimento di Farmacologia Preclinica e Clinica M. Aiazzi Mancini, Università degli Studi di Firenze, Viale G. Pieraccini 6, 50139 Firenze, Italia

2Biologie du Comportement, Université catholique de Louvain, 1 Place Croix du Sud, 1348 Louvain-la-Neuve, Belgium

3Chemistry Department, Huddersfield, UK

4Centre for Neuroinflammation & Neurodegeneration, Division of Brain Sciences, Faculty of Medicine, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK

*Corresponding Author:
Roberta J Ward
Biologie du Comportement, Université catholique de Louvain
1 Place Croix du Sud, 1348 Louvain-la-Neuve, Belgium
Tel: 003-210-456-004
E-mail: [email protected]

Received date: November 26, 2013; Accepted date: February 15, 2014; Published date: February 20, 2014

Citation: Stefanini C, Colivicchi MA, Della Corte L, Ward RJ, de Witte P, et al. (2014) Ethane-β-Sultam Modifies the Activation of the Innate Immune System Induced by Intermittent Ethanol Administration in Female Adolescent Rats. J Alcohol Drug Depend 2:150. doi: 10.4172/2329-6488.1000150

Copyright: © 2014 Stefanini C, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Intermittent ethanol abuse or ‘binge drinking’ during adolescence induces neuronal damage, which may be associated with cognitive dysfunction. To investigate the neurochemical processes involved, rats were administered either 1 g/kg or 2 g/kg ethanol in a ‘binge drinking’ regime. After only 3 weeks, significant activation of phagocytic cells in the peripheral (alveolar macrophages) and the hippocampal brain region (microglia cells) was present, as exemplified by increases in the release of pro-inflammatory cytokines in the macrophages and of iNOS in the microglia. This was associated with neuronal loss in the hippocampus CA1 region. Daily supplementation with a taurine prodrug, ethane-β-sultam, 0.028 g/kg, during the intermittent ethanol loading regime, supressed the release of the pro-inflammatory cytokines and of reactive nitrogen species, as well as neuronal loss, particularly in the rats administered the lower dose of ethanol, 1 g/kg. Plasma, macrophage and hippocampal taurine levels increased marginally after ethane-β-sultam supplementation. The ‘binge drinking’ ethanol rats administered 1 g/kg ethanol showed increased latencies to those of the control rats in their acquisition of spacial navigation in the Morris Water Maze, which was normalised to that of the controls values after ethane-β-sultam administration. Such results confirm that the administration of ethane-β-sultam to binge drinking rats reduces neuroinflammation in both the periphery and the brain, suppresses neuronal loss, and improved working memory of rats in a water maze study.


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