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Published Online: 8 July 2004

IL-1 Receptor Antagonist Prevents Apoptosis and Caspase-3 Activation after Spinal Cord Injury

Publication: Journal of Neurotrauma
Volume 18, Issue Number 9

Abstract

One of the consequences of cytokine-orchestrated inflammation after CNS trauma is apoptosis. Our hypothesis is that cell death in the spinal cord after injury results in part from increased synthesis and release of IL-1β. Using a ribonuclease protection assay, we demonstrated that there is increased transient expression of IL-1β mRNA and, by using IL-1β protein ELISA assay, that there are increased IL-1β protein levels in the contused rat spinal cord, initially localized to the impact region of the spinal cord (segment T8). Using an ELISA cell death assay, we showed that there is apoptosis in the spinal cord 72 h after injury, a finding that was confirmed by measuring caspase-3 activity, which also significantly increased at the site of injury 72 h after trauma. Treatment of the contused spinal cord at the site of injury with the IL-1 receptor antagonist (rmIL-1ra, 750 ng/mL) for 72 h using an osmotic minipump completely abolished the increases in contusion-induced apoptosis and caspase-3 activity.

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Published In

cover image Journal of Neurotrauma
Journal of Neurotrauma
Volume 18Issue Number 9September 2001
Pages: 947 - 956
PubMed: 11565605

History

Published online: 8 July 2004
Published in print: September 2001

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Olivera Nesic
Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, Texas
Guo-Ying Xu
Marine Biomedical Institute, University of Texas Medical Branch, Galveston, Texas
David McAdoo
Marine Biomedical Institute, University of Texas Medical Branch, Galveston, Texas
Karin Westlund High
Marine Biomedical Institute, and Department of Anatomy and Neurosciences, University of Texas Medical Branch, Galveston, Texas
Claire Hulsebosch
Marine Biomedical Institute, and Department of Anatomy and Neurosciences, University of Texas Medical Branch, Galveston, Texas
Regino Perez-Polo
Department of Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston, Texas

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