Introduction: Increasing studies have demonstrated that noninfectious inflammatory response could play a crucial role in second brain injury after traumatic brain injury(TBI). Despite its clinical significance and the extensive research efforts placed into elucidating its pathogenesis and therapy, the inflammatory response after TBI remains an incompletely understood and important clinical problem.The current study was intended to investigate the expression of CD24 in the cerebral cortex in a mouse closed head injury (CHI) model and to clarify the role of CD24 after CHI.
Methods: 56 mice were randomly divided into six groups: control group and CHI groups on day 1, 3, 5, 7, and 10. The mice in CHI groups suffered experimental CHI model and were sacrificed on day 1, 3, 5, 7, and 10, respectively. The expression of CD24 was assessed by quantitative real-time PCR, Western blot analysis and immunofluorence; and nuclear factor-kappa B (NF-kB) binding activity was detected by electrophoretic mobility shift assay (EMSA); and the levels of tumor necrosis factor-a (TNF-a) and Interleukin 1ß (IL-1ß) were measured by real-time PCR.
Results: The results showed that a progressive up-regulation of CD24 mRNA and protein occurred in the pericontusional cortex through day 5 and day 10 postinjury, with the peak on day 7. The expression of CD24 was elevated mainly in neurons and astrocytes rather than microglias, and CD24 immunoreactivity was observed mainly in the membrane of cells. NF-kB activity ascended significantly after CHI, reached the maximum on day 3. TNF-a and IL-1ß mRNA levels were markedly elevated following CHI on day 1, and then descended gradually with the time through day 3 and day 10.
Conclusions: Our results demonstrated that CD24 was increasingly expressed in a contrary time course to the up-regulation of NF-kB and proinflammatory cytokines. These findings might indicate the possible role of CD24 in the inflammatory response after CHI.
Patient Care: The results indicated that CD24 might play a key role in inflammatory response after TBI. Based on this research, we could further investigate the mechanisms of inflammatory response after TBI, which might finally benefit the patients with TBI.
Learning Objectives: By the conclusion of this session,participants should be able to:1)be clear of the expression of CD24 in cerebral cortex after TBI, 2)Describe the possible role of CD24 in inflammatory response following TBI, 3)yield a potential way to explore new therapeutic targets in patients with TBI.