Research on the effects and mechanisms of IL-17 on traumatic brain injury in rats

Objective: To investigate the effect and possible mechanism of IL-17 on traumatic brain injury (TBI) in rats. Methods: Seventy two healthy adult male Sprague-Dawley (SD) rats were randomly divided into three groups: sham operation group, TBI group, secukinumab (IL-17 inhibitor) and TBI group (S+T group). And each group was further divided into four subgroups (6 h, 12 h, 24 h and 48 h) of 6 rats on the basis of different observation times. TBI model was made by using the brain hydraulic impact method. In S+T group, secukinumab was intraperitoneally injected for 3 days in advance and TBI model was made at the specified observation time on the fourth day. In sham group, only craniotomy was performed. Neurological severity scores were applied in functional assessment of brain in each group; enzyme linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PT-PCR) method were applied to detect the contents of rat peripheral blood cytokines such as IL-6, TNF-alpha and IL-17 in each group; western blot (WB) was also applied to detect the level of I kappa B and p-P65 in brain tissues in each group. Results: Compared with shame group, ethology scores at each observation time, contents of cytokines (IL-6, TNF-alpha and IL-17) in peripheral blood, expressions of IL-6, TNF-alpha, IL-17 mRNA in brain tissues, degradation amount of I kappa B and expression of p-P65 were significantly increased in TBI group. In S+T group, however, the above indexes were between the sham group and TBI group (P < 0.05). Conclusion: Traumatic brain injury may be caused by IL-17 mediated activation of the downstream NF-kappa B pathway.