Expression of myeloid differentiation primary response protein 88 (Myd88) in the cerebral cortex after experimental traumatic brain injury in rats

摘要: Abstract A growing body of evidence indicates that Toll-like receptors (TLRs) and Interleukin-1 (IL-1) family have been shown to be involved in the damaging inflammatory processes associated with stroke, infection, neoplasia, other diseases central nervous system. Myeloid differentiation primary response protein 88 (Myd88) is a critical adaptor transmits signals for TLRs IL-1 family. Therefore, this study aimed detect expression Myd88 mRNA rat weight-dropping trauma model clarify role after traumatic brain injury (TBI). total fifty-four Sprague Dawley (SD) rats were randomly divided into control group TBI groups at hours 6, 12 on day 1, 2, 3, 7. The suffered experimental by improved Feeney model. measured Reverse Transcription PCR (RT-PCR), Western blot analysis immunohistochemistry; nuclear factor-kappaB (NF-κB) binding activity electrophoretic mobility shift assay (EMSA); levels tumor necrosis factor-α (TNF-α) Interleukin 1β (IL-1β) enzyme linked immunosorbent (ELISA) intercellular adhesion molecule-1 (ICAM-1) immunohistochemistry. injured was dramatically increased through 6 h 7 days postinjury, peaked 3 days. NF-κB, TNF-α, IL-1β ICAM-1 also ascended significantly TBI. Our data demonstrated increasingly expressed parallel time course up-regulation proinflammatory cytokines there highly positive relationship among them. These findings might important implications during administration specific antagonists order prevent or reduce