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Oxidative Stress as Secondary Injury Mechanism After Mechanical Trauma in the Spinal Cord

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Neuroprotection and Regeneration of the Spinal Cord

Abstract

The secondary pathological changes following mechanical trauma to the spinal cord cause deterioration of its function, and oxidative stress is known to contribute to the process. The roles of intercellular adhesion molecule-1 (ICAM-l) and nitric oxide in the process were investigated using rat incomplete spinal cord injury model.

ICAM-1mRNA expression reached its maximum at 6 h after SCI. By the intravenous injection of ICAM-1 monoclonal antibody (ICAM-l mAb) after SCI, posttraumatic polynuclear cell infiltration seemed to decrease and motor recovery was enhanced. Nitric oxide (NO) increased in the injured spinal cord. The expression of mRNA of constitutive NOS (c-NOS) did not change, whereas that of inducible NOS (i-NOS) increased after injury. Inhibiting the activity of c-NOS made motor function worse and that of i-NOS enhanced motor recovery.

Lecithinized superoxide dismutase (PC-SOD) was developed to increase half-life and permeability in vivo, and PC-SOD was used in this model to lessen oxidative stress. Intravenous injection of PC-SOD after injury suppressed the expression of IL-1β, ICAM-1, and i-NOS mRNAs, enhanced the expression of mRNA of neurotrophin-3, and caused motor recovery better than methylprednisolone injection.

These results indicated that oxidative stress enhances neuronal damage after mechanical trauma and suggested that it is important to suppress the oxidative stress.

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Katoh, S., Hamada, Y., Chikawa, T. (2014). Oxidative Stress as Secondary Injury Mechanism After Mechanical Trauma in the Spinal Cord. In: Uchida, K., Nakamura, M., Ozawa, H., Katoh, S., Toyama, Y. (eds) Neuroprotection and Regeneration of the Spinal Cord. Springer, Tokyo. https://doi.org/10.1007/978-4-431-54502-6_18

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  • DOI: https://doi.org/10.1007/978-4-431-54502-6_18

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