• Neuroscience · Jun 2016

    Unilateral microinjection of acrolein into thoracic spinal cord produces acute and chronic injury and functional deficits.

    • Alexander Gianaris, Nai-Kui Liu, Xiao-Fei Wang, Eddie Oakes, John Brenia, Thomas Gianaris, Yiwen Ruan, Ling-Xiao Deng, Maria Goetz, Sasha Vega-Alvarez, Qing-Bo Lu, Riyi Shi, and Xiao-Ming Xu.
    • Spinal Cord and Brain Injury Research Group, Stark Neurosciences Research Institute, Department of Neurological Surgery & Goodman Campbell Brain and Spine, Indiana University School of Medicine, Indianapolis, IN 46202, United States. Electronic address: redgianaris@gmail.com.
    • Neuroscience. 2016 Jun 21; 326: 84-94.

    AbstractAlthough lipid peroxidation has long been associated with spinal cord injury (SCI), the specific role of lipid peroxidation-derived byproducts such as acrolein in mediating damage remains to be fully understood. Acrolein, an α-β unsaturated aldehyde, is highly reactive with proteins, DNA, and phospholipids and is considered as a second toxic messenger that disseminates and augments initial free radical events. Previously, we showed that acrolein increased following traumatic SCI and injection of acrolein induced tissue damage. Here, we demonstrate that microinjection of acrolein into the thoracic spinal cord of adult rats resulted in dose-dependent tissue damage and functional deficits. At 24h (acute) after the microinjection, tissue damage, motoneuron loss, and spinal cord swelling were observed on sections stained with Cresyl Violet. Luxol fast blue staining further showed that acrolein injection resulted in dose-dependent demyelination. At 8weeks (chronic) after the microinjection, cord shrinkage, astrocyte activation, and macrophage infiltration were observed along with tissue damage, neuron loss, and demyelination. These pathological changes resulted in behavioral impairments as measured by both the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale and grid walking analysis. Electron microscopy further demonstrated that acrolein induced axonal degeneration, demyelination, and macrophage infiltration. These results, combined with our previous reports, strongly suggest that acrolein may play a critical causal role in the pathogenesis of SCI and that targeting acrolein could be an attractive strategy for repair after SCI.Copyright © 2016 IBRO. Published by Elsevier Ltd. All rights reserved.

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