[Che-1 participates in the regulation of rat cortical neuronal apoptosis and axonal regeneration after traumatic brain injury via p53].

Objective: To explore the altered expressions of Che-1 in rat brain cortex and relative biological functions after traumatic brain injury.

Methods: According to a random number table, a total of 64 male Sprague-Dawley rats were divided into normal, sham and trauma group. Then the trauma group was further divided into 6 phase sub-groups (12 h, 1 d, 3 d, 5 d, 7 d, 14 d) (n = 8 each). The craniocerebral injury (CCI) model was established to induce brain trauma at different time points. The examinations of Western blot and immunohistochemistry were performed to detect the expressions and diffusion changes of Che-1. Meanwhile the method of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) was employed to examine neuronal apoptosis. Additionally, the association of Che-1 with p53, active-caspase-3 and GAP43 was tested with Western blot and immunofluorescent staining.

Results: Compared with the normal and sham groups, the expression of Che-1 peaked at Day 3 post-injury (0.817 ± 0.022, P < 0.05) and it was related with neuronal apoptosis. Moreover, the altered expressions of p53, GAP43 and active-caspase-3 were associated with the level of Che-1.

Conclusion: The expression of Che-1 is elevated after brain trauma and may be involved in neuronal apoptosis and axonal regeneration through p53.