Erratum to: Inhibition of myeloperoxidase oxidant production by N-acetyl lysyltyrosylcysteine amide reduces brain damage in a murine model of stroke
| Autor: | Yu, Guoliang, Liang, Ye, Huang, Ziming, Jones, Deron W., Pritchard, Kirkwood A., Zhang, Hao |
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| Rok vydání: | 2016 |
| Předmět: |
Brain Infarction
Immunology Apoptosis Nitric Oxide Synthase Type I Motor Activity Mice Cellular and Molecular Neuroscience Animals Peroxidase Macrophages General Neuroscience Calcium-Binding Proteins Microfilament Proteins Infarction Middle Cerebral Artery Oxidants Mice Inbred C57BL Disease Models Animal Neuroprotective Agents Gene Expression Regulation Neutrophil Infiltration Neurology Blood-Brain Barrier Brain Injuries Microglia Erratum Tumor Suppressor Protein p53 Oligopeptides |
| Zdroj: | Journal of Neuroinflammation |
| ISSN: | 1742-2094 |
| DOI: | 10.1186/s12974-016-0639-y |
| Popis: | Oxidative stress plays an important and causal role in the mechanisms by which ischemia/reperfusion (I/R) injury increases brain damage after stroke. Accordingly, reducing oxidative stress has been proposed as a therapeutic strategy for limiting damage in the brain after stroke. Myeloperoxidase (MPO) is a highly potent oxidative enzyme that is capable of inducing both oxidative and nitrosative stress in vivo.To determine if and the extent to which MPO-generated oxidants contribute to brain I/R injury, we treated mice subjected to middle cerebral artery occlusion (MCAO) with N-acetyl lysyltyrosylcysteine amide (KYC), a novel, specific and non-toxic inhibitor of MPO. Behavioral testing, ischemic damage, blood-brain-barrier disruption, apoptosis, neutrophils infiltration, microglia/macrophage activation, and MPO oxidation were analyzed within a 7-day period after MCAO.Our studies show that KYC treatment significantly reduces neurological severity scores, infarct size, IgG extravasation, neutrophil infiltration, loss of neurons, apoptosis, and microglia/macrophage activation in the brains of MCAO mice. Immunofluorescence studies show that KYC treatment reduces the formation of chlorotyrosine (ClTyr), a fingerprint biomarker of MPO oxidation, nitrotyrosine (NO2Tyr), and 4-hydroxynonenal (4HNE) in MCAO mice. All oxidative products colocalized with MPO in the infarcted brains, suggesting that MPO-generated oxidants are involved in forming the oxidative products.MPO-generated oxidants play detrimental roles in causing brain damage after stroke which is effectively reduced by KYC. |
| Databáze: | OpenAIRE |
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