当前位置： SCI文献检索 > JOURNAL OF THE NEUROLOGICAL SCIENCES期刊下所有文献 > Blast-induced moderate neurotrauma (BINT) elicits early complement activation and tumor necrosis factor α (TNFα) release in a rat brain.

Blast-induced moderate neurotrauma (BINT) elicits early complement activation and tumor necrosis factor α (TNFα) release in a rat brain.

Abstract：

:Blast-induced neurotrauma (BINT) is a major medical concern yet its etiology is largely undefined. Complement activation may play a role in the development of secondary injury following traumatic brain injury; however, its role in BINT is still undefined. The present study was designed to characterize the complement system and adaptive immune-inflammatory responses in a rat model of moderate BINT. Anesthetized rats were exposed to a moderate blast (120 kPa) using an air-driven shock tube. Brain tissue injury, systemic and local complement, cerebral edema, inflammatory cell infiltration, and pro-inflammatory cytokine production were measured at 0.5, 3, 48, 72, 120, and 168 h. Injury to brain tissue was evaluated by histological evaluation. Systemic complement was measured via ELSIA. The remaining measurements were determined by immunohistoflourescent staining. Moderate blast triggers moderate brain injuries, elevated levels of local brain C3/C5b-9 and systemic C5b-9, increased leukocyte infiltration, unregulated tumor necrosis factor alpha (TNFα), and aquaporin-4 in rat brain cortex at 3- and 48-hour post blast. Early immune-inflammatory response to BINT involves complement and TNFα, which correlates with hippocampus and cerebral cortex damage. Complement and TNFα activation may be a novel therapeutic target for reducing the damaging effects of BINT inflammation.

journal_name

J Neurol Sci

journal_title

Journal of the neurological sciences

authors

Dalle Lucca JJ,Chavko M,Dubick MA,Adeeb S,Falabella MJ,Slack JL,McCarron R,Li Y

doi

10.1016/j.jns.2012.02.002

subject

Has Abstract

pub_date

2012-07-15 00:00:00

pages

146-54

issue

1-2

eissn

0022-510X

issn

1878-5883

pii

S0022-510X(12)00059-7

journal_volume

318

pub_type

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