The role of interleukin-17A in the inflammatory response after traumatic brain injury in rats

Abstract

Objective To investigate the role and potential mechanism of interleukin-17A(IL-17A) in the inflammatory response to traumatic brain injury (TBI) in rats. Methods The adult male Wistar rats were randomly(random number) divided into seven groups: control group (n=6), sham operation group (n=6), TBI group (n=24), sham operation + normal saline group (n=6), sham operation + Y320 (an immunomodulator acts as an inhibitor of IL-17A) group (n=6), TBI + normal saline group (n=6) and TBI+ Y320 group (n=6). The TBI model of rat was established by using free-falling-body impact device. The levels of IL-17A and nuclear transcription factor kappa B p65 (NF-κB p65) in the cerebral cortex were assayed by using Western Blot. The capability of learning and memory of rats was assessed by Morris water maze. The beam balance test was employed to evaluating the neurological motor performance and the capability of balance. Results Compared with the sham operation group, the levels of IL-17A and NF-κB p65 in the cerebral cortex of TBI, TBI + saline and TBI + Y320 groups increased significantly (P<0.05) and peaked at the 3rd day after TBI. Compared with TBI + normal saline group, the level of NF-κB p65 was significantly down regulated by Y-320 (P<0.05) at the 3rd day after TBI in TBI+ Y320 group. The lengths of latency time required for rats to escape to the platform area in TBI + normal saline group were (57.72±3.29)s, (55.63±3.85)s, and (55.02±3.92)s at the 3rd, 5th and 7th days after TBI, respectively; while those in TBI+ Y320 group were (35.45±3.04)s, (30.98±2.92)s, and (23.90±2.51)s at the 3rd, 5th and 7th days after TBI, respectively. Thus, the capability of learning and memory of rats in TBI+ Y320 group was improved significantly 3d, 5d and 7 days after TBI (all P<0.01). Conclusions This study shows IL-17A is involved in the process of secondary brain injury after TBI, and associated with inflammation by activating the NF-κB p65 signaling pathway. Key words: Traumatic brain injury; IL-17A; NF-κB p65; Y320; Inflammatory response; Cytokine; Rats