Journal
EUROPEAN JOURNAL OF INFLAMMATION
Volume 15, Issue 2, Pages 78-84Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/1721727X17706855
Keywords
brain; inflammation; ischemia; microglia; necroptosis
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Funding
- Natural Science Foundation of China (NSFC) [81472150]
- Key Projects of Shanghai Science and Technology on Biomedicine [13411951000]
- Key Construction Projects of Shanghai Health and Family Planning on Weak Discipline [2015ZB0401]
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Microglia, which are the resident macrophages and the first line of defense in the brain, can be activated within hours and migrate toward the injury sites after acute and chronic ischemic brain injury. However, a few studies have reported the interaction between microglia activation and necroptosis signaling following ischemic damage to the brain. In this study, chronic ischemic brain injury was induced by bilateral carotid artery stenosis (BCAS) and mice were sacrificed at 30 days after surgery. Ionized calcium-binding adaptor molecule 1 (IBA1) and glial fibrillary acidic protein (GFAP) immunostaining were performed to determine glial cell activation and inflammatory response. Tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (INF-gamma), and interleukin-1 beta (IL-1 beta) proteins from the brains were examined to confirm inflammatory cytokines after BCAS. RIP1 and RIP3 proteins were detected to determine necroptosis signaling by Western blot. The data suggested that inflammatory responses, microglia activation, and necroptosis signaling are features of brain tissue pathology following BCAS-induced chronic ischemic brain injury.
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