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BioMed Research International
Volume 2013 (2013), Article ID 827517, 8 pages
http://dx.doi.org/10.1155/2013/827517
Research Article

Immunization with a Neural-Derived Peptide Protects the Spinal Cord from Apoptosis after Traumatic Injury

1Facultad de Ciencias de la Salud, Universidad Anáhuac México Norte, Edo. de México, CP 52786, Mexico
2Departamento de Ciencias de la Salud, División de Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana Iztapalapa, DF, CP 09340, Mexico
3Centro de Investigación del Proyecto CAMINA A.C., DF, CP 14050, Mexico
4Posgrado en Biología Experimental, Universidad Autónoma Metropolitana Iztapalapa, DF, CP 09340, Mexico
5Departamento de Microbiología y Parasitología, Facultad de Medicina, UNAM, DF, CP 04510, Mexico

Received 1 May 2013; Revised 23 August 2013; Accepted 6 September 2013

Academic Editor: Johan Pallud

Copyright © 2013 Roxana Rodríguez-Barrera 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

Apoptosis is one of the most destructive mechanisms that develop after spinal cord (SC) injury. Immunization with neural-derived peptides (INDPs) such as A91 has shown to reduce the deleterious proinflammatory response and the amount of harmful compounds produced after SC injury. With the notion that the aforementioned elements are apoptotic inducers, we hypothesized that INDPs would reduce apoptosis after SC injury. In order to test this assumption, adult rats were subjected to SC contusion and immunized either with A91 or phosphate buffered saline (PBS; control group). Seven days after injury, animals were euthanized to evaluate the number of apoptotic cells at the injury site. Apoptosis was evaluated using DAPI and TUNEL techniques; caspase-3 activity was also evaluated. To further elucidate the mechanisms through which A91 exerts this antiapoptotic effects we quantified tumor necrosis factor-alpha (TNF-α). To also demonstrate that the decrease in apoptotic cells correlated with a functional improvement, locomotor recovery was evaluated. Immunization with A91 significantly reduced the number of apoptotic cells and decreased caspase-3 activity and TNF-α concentration. Immunization with A91 also improved the functional recovery of injured rats. The present study shows the beneficial effect of INDPs on preventing apoptosis and provides more evidence on the neuroprotective mechanisms exerted by this strategy.