Annexin A1 reduces inflammatory reaction and tissue damage through inhibition of phospholipase A2 activation in adult rats following spinal cord injury
Autor: | Lisa Y. Xu, Shu Han, Naikui Liu, Yi Ping Zhang, Pei Hua Lu, Christopher B. Shields, Xiao Ming Xu, Jiong Pei |
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Rok vydání: | 2007 |
Předmět: |
endocrine system
Stilbamidines Cell Survival Blotting Western Pharmacology Phospholipase Motor Activity Neuroprotection Phospholipases A Pathology and Forensic Medicine Rats Sprague-Dawley Cellular and Molecular Neuroscience Phospholipase A2 medicine Animals Gliosis Spinal cord injury Cells Cultured Injections Spinal Spinal Cord Injuries Annexin A1 Peroxidase Inflammation Phospholipase A Glial fibrillary acidic protein biology General Medicine medicine.disease Spinal cord Evoked Potentials Motor Rats Electrophysiology Enzyme Activation Phospholipases A2 medicine.anatomical_structure Neurology Spinal Cord Immunology biology.protein Female Neurology (clinical) |
Zdroj: | Journal of neuropathology and experimental neurology. 66(10) |
ISSN: | 0022-3069 |
Popis: | Annexin A1 (ANXA1) has been suggested to be a mediator of the anti-inflammatory actions of glucocorticoids and more recently an endogenous neuroprotective agent. In the present study, we investigated the anti-inflammatory and neuroprotective effects of ANXA1 in a model of contusive spinal cord injury (SCI). Here we report that injections of ANXA1 (Ac 2-26) into the acutely injured spinal cord at 2 concentrations (5 and 20 microg) inhibited SCI-induced increases in phospholipase A2 and myeloperoxidase activities. In addition, ANXA1 administration reduced the expression of interleukin-1beta and activated caspase-3 at 24 hours, and glial fibrillary acidic protein at 4 weeks postinjury. Furthermore, ANXA1 administration significantly reversed phospholipase A2-induced spinal cord neuronal death in vitro and reduced tissue damage and increased white matter sparing in vivo, compared to the vehicle-treated controls. Fluorogold retrograde tracing showed that ANXA1 administration protected axons of long descending pathways at 6 weeks post-SCI. ANXA1 administration also significantly increased the number of animals that responded to transcranial magnetic motor-evoked potentials. However, no measurable behavioral improvement was found after these treatments. These results, particularly the improvements obtained in tissue sparing and electrophysiologic measures, suggest a neuroprotective effect of ANXA1. |
Databáze: | OpenAIRE |
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