AI Article Synopsis
- Inflammatory responses play a significant role in causing damage after traumatic brain injury (TBI).
- Researchers studied the expression of key proinflammatory molecules in rats following closed head injury (CHI), observing a spike in certain cytokine levels shortly after the trauma.
- Key findings indicated that while proinflammatory molecules (IL-1beta, IL-6, TNF-alpha) increased rapidly within hours after injury, their levels dropped back toward baseline by 24 hours, suggesting a complex healing process that could impact areas beyond the initial injury site.
Article Abstract
Inflammatory processes have been implicated in the pathogenesis of traumatic brain damage. We analyzed the spatiotemporal expression pattern of the proinflammatory key molecules: interleukin-1beta, interleukin-6, tumor necrosis factor-alpha, and inducible nitric oxide synthase in a rat closed head injury (CHI) paradigm. 51 rats were used for RT-PCR analysis after CHI, and 18 for immunocytochemistry. We found an early upregulation of IL-1beta, IL-6, and TNF-alpha mRNA between 1h and 7h after injury; the expression of iNOS mRNA only revealed a significant increase at 4h. After 24h, the expression decreased towards baseline levels, and remained low until 7d after injury. Immunocytochemically, IL-1beta induction was localized to ramified microglia in areas surrounding the primary impact place as well as deeper brain structures. Our study shows rapid induction of inflammatory gene expression that exceeds by far the primary impact site and might therefore contribute to tissue damage at remote sites.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1570383 | PMC |
| http://dx.doi.org/10.1155/MI/2006/90123 | DOI Listing |
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