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- W2137620233 abstract "Traumatic brain injury (TBI) can cause gastrointestinal dysfunction and increase intestinal permeability. Nuclear factor kappa B (NF-κB) has been shown to be associated with these intestinal events, but it is not well known how NF-κB is activated in the intestine after TBI. Based on previous studies, we hypothesize that myeloid differentiation primary response protein 88 (Myd88) may have an important role in NF-κB activation in the intestine, which mediates the inflammation and ultimately results in acute intestinal mucosal injury.We randomly divided adult male C57BL/6 mice into control groups and TBI groups at different time points. We induced a closed head injury model by weight drop (a 333-g metal rod dropping from a 2.5-cm height). We detected Myd88 protein level and NF-κB binding activity in ileum tissue by Western blot and electrophoretic mobility shift assay, respectively. Meanwhile, we detected the mRNA levels of Myd88, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and intercellular adhesion molecule-1 by real-time polymerase chain reaction.The Myd88 protein and mRNA levels, as well as NF-κB binding activity in the ileum tissue, significantly increased at 6 h after TBI, peaked at 3 d, and remained elevated by 5 d post-injury. The levels of TNF-α, IL-1β, and intercellular adhesion molecule-1 also remarkably increased after TBI. There was a positive relationship between the expression of Myd88 and that of NF-κB, TNF-α, and IL-1β.Traumatic brain injury induced a rapid and persistent up-regulation of Myd88, NF-κB, and proinflammatory cytokines in the intestine. This up-regulation which might have an important role in the pathogenesis of acute intestinal mucosal injury." @default.
- W2137620233 created "2016-06-24" @default.
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- W2137620233 date "2013-01-01" @default.
- W2137620233 modified "2023-09-22" @default.
- W2137620233 title "Expression of intestinal myeloid differentiation primary response protein 88 (Myd88) following experimental traumatic brain injury in a mouse model" @default.
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- W2137620233 doi "https://doi.org/10.1016/j.jss.2012.03.030" @default.
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