Beta2-adrenoreceptor agonist-enhanced recovery of locomotor function after spinal cord injury is glutathione dependent

Journal of Neurotrauma
R J ZemanJ D Etlinger

Abstract

The beta2-adrenoreceptor agonist, clenbuterol, has been shown to spare spinal cord tissue and enhance locomotor recovery in an experimental model of spinal cord contusion injury. A likely mechanism of neurodegeneration following spinal cord injury involves generation of toxic levels of reactive oxygen species (ROS), e.g., O2-*, H2O2 and OH*, which overwhelm endogenous antioxidants. Agents, such as clenbuterol, that oppose neurodegeneration and improve recovery of locomotor function may possibly act by improving redox status. Consistent with reduced oxidative stress by beta2-agonist treatment following injury, prior blockade of synthesis of the antioxidant tripeptide, glutathione, with buthionine sulfoximine completely inhibited the ability of clenbuterol to enhance locomotor recovery and spare spinal cord tissue. Moreover, at 8 h postinjury, clenbuterol caused an increase in glutathione reductase activity, an indicator of cellular redox status, at the injury site that was also blocked by buthionine sulfoximine. Although clenbuterol improved locomotor recovery only when administered within a therapeutic window of several days postinjury, the accumulation of protein carbonyls in the spinal cord at 1 week postinjury, a consequence...Continue Reading

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Citations

Jun 17, 2010·Pflügers Archiv : European journal of physiology·Fusheng BaiRichard J Zeman
May 9, 2009·Neuroreport·Richard J ZemanChristopher P Cardozo
Nov 14, 2008·Neurosurgery·Richard J ZemanJoseph D Etlinger
Feb 22, 2011·The Journal of Immunology : Official Journal of the American Association of Immunologists·Li QianPatrick M Flood

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