| Objectives To investigate the expression of NF-κB,tumor necrosis factor-alpha(TNF-α) and interleukin-6(IL-6) after traumatic brain injury, and if the secondary brain injury would decrease when the expression of NF-κB was inhibited, in order to provide the theoretical basis directly for a new approach to the clinical management of traumatic brain injury.Methods The free-falling-body impact device was used to cause the models of local moderate contusion and laceration in the rats. Seventy Wistar rats weighing 250-300g were randomly divided into four groups: normal group(n=10),injury group(n=20)and treatment group(n=40).Both injuries and treatment with pyrro-lidinedithiocarbamate(PDTC) and dexamethasone were given to the treatment group. The control group only received injuries and neither was given to the normal group. Rats of injury group and treatment group were killed at 6h,24h,72h,120h after injury respectively. The injured brain tissue were fixed by paraformaldehyde and embedded paraffin and then sliced. Using immunohistochemistry in situ detection, A investigation was made to discover the relationship between the expression of NF-κB,TNF-αafter traumatic brain injury and the secondary brain injury. IL-6 was inspected using ELISA.Results No immuno-reactivity for NF-κB,TNF-αwas observed in normal group animals at any survival time. IL-6 was lower. In the neurodegenerative area surrounding the lesion of injury group,a significative increase in NF-κB and TNF-αimmunoreactivity was observed from 6h to 120h. In contrast, inflammatory cells infiltration in trial group was effectively suppressed when the expression of NF-κB,TNF-αwas significantly downregulated.Conclusion The study shows the activation of NF-κB,TNF-αmay be the important mechanism of acute traumatic brain injury with acute inflammation. These findings suggest that the application of NF-kappaB inhibitor may be a potential therapeutic method for the treatment of brain inflammatory reaction after traumatic brain injury.
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