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Indexed/Abstracted in: e-psyche, EMBASE, PubMed/MEDLINE, Neuroscience Citation Index, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,651
Online ISSN 1827-1855
Conti A. 1, Cardali S. 1, Genovese T. 2, Di Paola R. 2, La Rosa G. 1
1 Neurosurgical Clinic, University of Messina School of Medicine, Messina, Italy
2 Institute of Pharmacology, University of Messina School of Medicine, Messina, Italy
Aim. The primary traumatic mechanical injury to the spinal cord causes the death of a number of neurons that cannot be recovered, neither regenerated. However, neurons continue to die for hours after spinal cord injury (SCI), and this represents a potentially avoidable event. One of mechanisms that have been touted to contribute importantly to the evolution of such secondary cell death is the local inflammatory response in the injured spinal cord. In this report we have used an in vivo model to induce acute SCI and reproduce the acute pathological events associated with inflammation after traumatic SCI in rats.
Methods. Twenty-two adult male Sprague-Dawley rats were used in the study. SCI was produced by extradural clip compression at T5-T9 level. The rats spinal cord was analysed at 1 hour to measure the malonildialdehyde (MDA) levels considered an index of lipid peroxidation. At 4 hours were measured the levels of myeloperoxidase (MPO) activity considered as the index of leukocytes activity. Finally the spinal cord was extracted 12 hours after the trauma to measure the cytoplasmatic levels of IκB-α considered as the index of activity of the transcriptional factor nuclear factor-κB (NF-κB).
Results. After the SCI, both the levels of MDA and MPO were significantly higher compared with naive and sham-operated rats (p=0.01). Western blotting analysis demonstrated the disappearance of IκB-α in the cytoplasm indicating nuclear translocation of the NF-κB.
Conclusion. The study confirms the role of inflammation in contributing to the secondary injury after experimental SCI in the rat.