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N-acetylcysteine reduces lipopolysaccharide-sensitized hypoxic-ischemic brain injury.

Journal article
Authors Xiaoyang Wang
Pernilla Svedin
Chunxia Nie
Risto Lapatto
Changlian Zhu
Malin Gustavsson
Mats Sandberg
Jan-Olof Karlsson
Roberto Romero
Henrik Hagberg
Carina Mallard
Published in Annals of neurology
Volume 61
Issue 3
Pages 263-71
ISSN 0364-5134
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Institute of Clinical Sciences
Pages 263-71
Language en
Links dx.doi.org/10.1002/ana.21066
Keywords Animals, Animals, Newborn, Apoptosis, drug effects, Calpain, drug effects, Caspases, drug effects, Cystine, analogs & derivatives, pharmacology, Enzyme Activation, drug effects, Glutathione, drug effects, Hypoxia-Ischemia, Brain, chemically induced, prevention & control, Isoprostanes, metabolism, Lipopolysaccharides, toxicity, Membrane Proteins, drug effects, Neuroprotective Agents, pharmacology, Oxidation-Reduction, drug effects, Rats, Rats, Wistar, Thioredoxin, drug effects, Tyrosine, analogs & derivatives, drug effects
Subject categories Medical and Health Sciences

Abstract

OBJECTIVE: Maternal inflammation/infection alone or in combination with birth asphyxia increases the risk for perinatal brain injury. Free radicals are implicated as major mediators of inflammation and hypoxia-ischemia (HI)-induced perinatal brain injury. This study evaluated the neuroprotective efficacy of a scavenging agent, N-acetylcysteine (NAC), in a clinically relevant model. METHODS: Lipopolysaccharide (LPS)-sensitized HI brain injury was induced in 8-day-old neonatal rats. NAC was administered in multiple doses, and brain injury was evaluated at 7 days after HI. RESULTS: NAC (200mg/kg) provided marked neuroprotection with up to 78% reduction of brain injury in the pre+post-HI treatment group and 41% in the early (0 hour) post-HI treatment group, which was much more pronounced protection than another free radical scavenger, melatonin. Protection by NAC was associated with the following factors: (1) reduced isoprostane activation and nitrotyrosine formation; (2) increased levels of the antioxidants glutathione, thioredoxin-2, and (3) inhibition of caspase-3, calpain, and caspase-1 activation. INTERPRETATION: NAC provides substantial neuroprotection against brain injury in a model that combines infection/inflammation and HI. Protection by NAC was associated with improvement of the redox state and inhibition of apoptosis, suggesting that these events play critical roles in the development of lipopolysaccharide-sensitized HI brain injury.

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