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Newer pharmacological approaches for antioxidant neuroprotection in traumatic brain injury.
Neuropharmacology
February 2019
Spinal Cord & Brain Injury Research Center and Department of Neuroscience, University of Kentucky College of Medicine, Lexington, KY 40536-0509, USA.
Reactive oxygen species-induced oxidative damage remains an extensively validated secondary injury mechanism in traumatic brain injury (TBI) as demonstrated by the efficacy of various pharmacological antioxidants agents in decreasing post-traumatic free radical-induced lipid peroxidation (LP) and protein oxidative damage in preclinical TBI models. Based upon strong preclinical efficacy results, two antioxidant agents, the superoxide radical scavenger polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) and the 21-aminosteroid LP inhibitor tirilazad, which inhibits lipid peroxidation, (LP) were evaluated in large phase III trials in moderately- and severely-injured TBI patients. Both failed to improve 6 month survival and neurological recovery.
View Article and Find Full Text PDFOxidative stress in spinal cord injury and antioxidant-based intervention.
Spinal Cord
April 2012
Department of Biology, University of North Carolina at Greensboro, Greensboro, NC, USA.
Study Design: Literature review.
Objectives: Spinal cord injury (SCI) remains a major public health issue in developed countries as well as worldwide. The pathophysiology of SCI is characterized by an initial primary injury followed by secondary deterioration.
Neuroprotection and acute spinal cord injury: a reappraisal.
NeuroRx
January 2004
Spinal Cord and Brain Injury Research Center, University of Kentucky Chandler Medical Center, Lexington, Kentucky 40536, USA.
It has long been recognized that much of the post-traumatic degeneration of the spinal cord following injury is caused by a multi-factorial secondary injury process that occurs during the first minutes, hours, and days after spinal cord injury (SCI). A key biochemical event in that process is reactive oxygen-induced lipid peroxidation (LP). In 1990 the results of the Second National Acute Spinal Cord Injury Study (NASCIS II) were published, which showed that the administration of a high-dose regimen of the glucocorticoid steroid methylprednisolone (MP), which had been previously shown to inhibit post-traumatic LP in animal models of SCI, could improve neurological recovery in spinal-cord-injured humans.
View Article and Find Full Text PDFDrug development in spinal cord injury: what is the FDA looking for?
J Rehabil Res Dev
May 2004
Spinal Cord and Brain Injury Research Center, University of Kentucky Chandler Medical Center, Lexington, KY 40515, USA.
It has long been recognized that much of the post-traumatic degeneration of the spinal cord following injury is caused by a secondary injury process that occurs during the first minutes, hours, and days after spinal cord injury (SCI). A key biochemical event in that process is reactive oxygen-induced lipid peroxidation (LP). Indeed, the administration of a high-dose regimen of the glucocorticoid steroid methylprednisolone (MP) has been shown to inhibit post-traumatic LP in animal models of SCI, and to improve neurological recovery in spinal cord-injured humans.
View Article and Find Full Text PDF[Effects of U74389G on pulmonary macrophage influx and lung development in 95% O2 exposed newborn rats].
Zhonghua Er Ke Za Zhi
February 2004
Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Objective: Oxygen toxicity is believed to play a critical role in the pathogenesis of bronchopulmonary dysplasia (BPD). U74389G, a potent 21-aminosteroid antioxidant, was applied to the 95% O(2) induced acute lung injury in newborn rat model. The present study aimed to investigate the mechanism of hyperoxic lung injury and the interaction of possible mediators, and to explore the effect of antioxidant intervention.
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