期刊
JOURNAL OF NEUROCHEMISTRY
卷 136, 期 5, 页码 1017-1025出版社
WILEY
DOI: 10.1111/jnc.13491
关键词
ApoJ; complement cascade; oxidative stress; TBI
资金
- National Natural Science Foundation of China [81371378]
- National Construction Project for Clinical Key Specialty [(2011)170]
- Guizhou Science and Technology Department [(2013)2332]
Traumatic brain injury (TBI) is the leading cause of mortality and morbidity in youth, but to date, effective therapies are still lacking. Previous studies revealed a marked response of apolipoprotein J (ApoJ) expression to the brain injury. The aim of this study was to determine the potential roles of ApoJ in functional recovery following TBI. After controlled cortex impact (CCI), a TBI model, in adult wild-type mice, ApoJ expression was up-regulated since 6h post-injury and sustained for 5days. Animals infused with recombinant human ApoJ intraventricularly at 30min prior to CCI showed significantly reduced oxidative stress (3-nitrotyrosine, 4-hydroxynonenal) and complement activation (C5b-9). In addition, ApoJ treatment was shown to suppress the inflammatory response (glial activation, cytokine expression), blood-brain barrier disruption (Evans blue extravasation), and cerebral edema (water content) induced by CCI. Concomitantly, improved neuronal maintenance and neurological behavioral performance were observed in ApoJ-treated mice compared with the vehicle group. These findings support a neuroprotective role of ApoJ via multifunctional pathways, providing a novel and encouraging treatment strategy for TBI.
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