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- Title
Biphasic activation of nuclear factor kappa B and expression of p65 and c-Rel after traumatic brain injury in rats.
- Authors
Hu, Yang-Chun; Sun, Qing; Li, Wei; Zhang, Ding-Ding; Ma, Biao; Li, Song; Li, Wei-De; Zhou, Meng-Liang; Hang, Chun-Hua
- Abstract
Background and object: Nuclear factor kappa B (NF-κB) functions as a key regulator in the central nervous system and regulates the inflammatory pathway. There are two peaks of cerebral NF-κB activation after neonatal hypoxia-ischemia and subarachnoid hemorrhage. Our previous studies found that NF-κB activity was up-regulated at an early stage and remained elevated at day 7 after traumatic brain injury (TBI). However, data are lacking regarding an overview of NF-κB activity and expression of NF-κB subunits after TBI. Hence, the current study was designed to detect the time course of NF-κB activation and expression of NF-κB p65 and c-Rel subunits around the contused cortex following TBI. Methods: Adult Sprague-Dawley rats were randomly divided into sham and TBI groups at different time points. A TBI model was induced, and then the NF-κB DNA-binding activity in the surrounding areas of injured brain was detected by electrophoretic mobility shift assay. Western blotting was used to measure the protein levels of p65 and c-Rel in the nucleus. The concentrations of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were detected by enzyme-linked immunosorbent assay. Moreover, the distribution of c-Rel and p65 was examined by immunohistochemical studies. Results: There were double peaks of cerebral cortical NF-κB activity, at 3 and 10 days post-injury. Additionally, protein levels of p65 were found to be elevated and peaked at 3 days after TBI, while levels of c-Rel were elevated significantly during the later phase of injury. Furthermore, TNF-α and IL-1β concentrations also showed a biphasic increase. Conclusions: Biphasic activation of NF-κB could be induced after experimental TBI in rats. NF-κB p65 and c-Rel subunits were elevated at different post-TBI time periods, leading to a hypothesis that different NF-κB subunits might be involved in different pathophysiological processes after TBI.
- Subjects
NF-kappa B; GENE expression; BRAIN injuries; PROTO-oncogenes; INFLAMMATION; HYPOXEMIA; ISCHEMIA
- Publication
Inflammation Research, 2014, Vol 63, Issue 2, p109
- ISSN
1023-3830
- Publication type
Article
- DOI
10.1007/s00011-013-0677-1