Open Access
J Brachial Plex Peripher Nerve Inj 2007; 02(01): e91-e94
DOI: 10.1186/1749-7221-2-3
Short report
Subbanna et al; licensee BioMed Central Ltd.

Acetyl salicylic acid augments functional recovery following sciatic nerve crush in mice[*]

Prasanna Kumar T Subbanna
1   Department of Pharmacology & Clinical Pharmacology, Christian Medical College, Vellore-632002, India
,
CG Prasanna
1   Department of Pharmacology & Clinical Pharmacology, Christian Medical College, Vellore-632002, India
,
Bhagawat K Gunale
1   Department of Pharmacology & Clinical Pharmacology, Christian Medical College, Vellore-632002, India
,
Manoj G Tyagi
1   Department of Pharmacology & Clinical Pharmacology, Christian Medical College, Vellore-632002, India
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Publikationsverlauf

04. Dezember 2006

04. Februar 2007

Publikationsdatum:
17. September 2014 (online)

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Abstract

Cyclin-dependent kinase 5 (CDK-5) appears to play a significant role in peripheral nerve regeneration as CDK-5 inhibition retards nerve regeneration following nerve crush. Anti-inflammatory drug acetyl salicylic acid elevates CDK-5 and reduces ischemia – reperfusion injury in cultured neurons. In this study we have evaluated the effect of acetyl salicylic acid on functional recovery following sciatic nerve crush in mice. Eighteen Swiss albino mice underwent unilateral sciatic nerve crush. Test animals received acetyl salicylic acid (100 mg/kg/day, n = 6 or 50 mg/kg/day, n = 6) and control animals (n = 6) received normal saline for 14 days following surgery. Functional recovery was assessed with improvement in Sciatic Function Index, nociception and gait. In comparison with normal saline treatment, acetyl salicylic acid (100 mg/kg/day) significantly improved functional recovery following sciatic nerve crush. Anti-inflammatory drug acetyl salicylic acid appears to be a promising agent for treating peripheral nerve injuries and hence elucidation of its neuroprotective pathways is necessary.

*This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.