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Updated: May 11, 2026
Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Expression of intestinal CD40 after experimental traumatic brain injury in rats
Yang-Chun Hu1, Fan Wang, Ding-Ding Zhang
1Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu Province, People's Republic of China; Department of Neurosurgery, Affiliated Hospital of Guiyang Medical College, Guiyang, Guizhou Province, People's Republic of China.
Background:
Nuclear factor kappa B (NF-κB) has been shown to be activated in the intestine after traumatic brain injury (TBI), and results in gastrointestinal mucosal injury. In addition, CD40 has a major role in the activation of NF-κB and is up-regulated in inflammatory bowel disease. However, we found no study in the literature investigating the intestinal expression of CD40 after TBI. Hence, we designed the current study to explore the intestinal expression pattern of CD40 after TBI in rats. We hypothesized that CD40 could mediate inflammation and ultimately contribute to acute intestinal mucosal injury after TBI.
Methods:
We randomly divided rats into control and TBI groups at 3, 6, 12, 24, and 72 h, respectively. We assessed the expression of CD40 by quantitative real-time polymerase chain reaction, Western blotting, and immunohistochemical study, and detected the levels of tumor necrosis factor-α (TNF-α), intracellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) by enzyme-linked immunosorbent assay.
Results:
The mRNA and protein levels of -CD40 increased by 3 and 6 h, peaked at 6 and 12 h, and remained elevated until 24 and 72 h post-injury, respectively. Levels of TNF-α, VCAM-1, and ICAM-1 also markedly increased in jejunum tissue after TBI. Interestingly, there was a positive relationship between the expression of CD40 and that of TNF-α, VCAM-1, and ICAM-1.
Conclusions:
CD40 could be markedly elevated in intestine after TBI in rats, and it might have an important role in the pathogenesis of acute intestinal mucosal injury mediated by inflammatory response.
