Immunization with a neural-derived peptide protects the spinal cord from apoptosis after traumatic injury
- Roxana Rodríguez-Barrera,
- Ana M. Fernández-Presas,
- Elisa García,
- Adrian Flores-Romero,
- Susana Martiñón,
- Viridiana Yazmín González-Puertos
- Universidad Autónoma Metropolitana,
- Instituto Mexicano del Seguro Social,
- Universidad Anáhuac,
- Universidad Nacional Autónoma de México,
- ,
Open access
Publication Information
Output type
Original language
EnglishArticle number
827517Journal (Volume, Issue Number)
BioMed Research International (Volume 2013)Publication milestones
- Published - 18/11/2013
Publication status
ISSN
2314-6133Publication IDs
- Scopus: 84887496710
- PubMed: 24236295
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.
