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BioMed Research International
Volume 2013 (2013), Article ID 985093, 14 pages
http://dx.doi.org/10.1155/2013/985093
Research Article

Neuroprotective Activity of Thioctic Acid in Central Nervous System Lesions Consequent to Peripheral Nerve Injury

1School of Bioscience and Biotechnology, University of Camerino, Via Gentile III da Varano, 62032 Camerino, Italy
2School of Medicinal and Health Products Sciences, University of Camerino, Via Madonna delle Carceri, 9, 62032 Camerino, Italy
3Department of Clinical and Preclinical Pharmacology, University of Florence, Viale Pieraccini, 6, 50134 Florence, Italy
4Department of Anatomy, Histology and Forensic Medicine, University of Florence, Largo Brambilla, 1, 50134 Florence, Italy

Received 7 August 2013; Revised 25 November 2013; Accepted 25 November 2013

Academic Editor: Swaran J. S. Flora

Copyright © 2013 Daniele Tomassoni et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Peripheral neuropathies are heterogeneous disorders presenting often with hyperalgesia and allodynia. This study has assessed if chronic constriction injury (CCI) of sciatic nerve is accompanied by increased oxidative stress and central nervous system (CNS) changes and if these changes are sensitive to treatment with thioctic acid. Thioctic acid is a naturally occurring antioxidant existing in two optical isomers (+)- and (−)-thioctic acid and in the racemic form. It has been proposed for treating disorders associated with increased oxidative stress. Sciatic nerve CCI was made in spontaneously hypertensive rats (SHRs) and in normotensive reference cohorts. Rats were untreated or treated intraperitoneally for 14 days with (+/−)-, (+)-, or (−)-thioctic acid. Oxidative stress, astrogliosis, myelin sheets status, and neuronal injury in motor and sensory cerebrocortical areas were assessed. Increase of oxidative stress markers, astrogliosis, and neuronal damage accompanied by a decreased expression of neurofilament were observed in SHR. This phenomenon was more pronounced after CCI. Thioctic acid countered astrogliosis and neuronal damage, (+)-thioctic acid being more active than (+/−)- or (−)-enantiomers. These findings suggest a neuroprotective activity of thioctic acid on CNS lesions consequent to CCI and that the compound may represent a therapeutic option for entrapment neuropathies.