Role of TLR4/NF-kB signal pathway in rat nerve injury after traumatic brain injury coupled with seawater drowning

Abstract

Objective To explore the role of TLR4/NF-kB signal pathway in rat nerve injury after traumatic brain injury coupled with seawater drowning. Methods A total of 96 male Sprague-Dawley rats were randomly divided into 3 groups: the sham surgery group(n=12), the traumatic brain injury (TBI) group(n=42)and the traumatic brain injury coupled with seawater drowning group (or the TBI + SWD group)(n=42). At the timepoints of 3, 6, 12, 24, 72 and 168 hours after the establishment of the TBI model, immunohistochemistry was used to detect the expression of TLR4 and NF-kB cells in the rat brain tissue. Real time PCR (rt-PCR) was applied to detect the expression levels of TLR4 and NF-kB mRNA in the hippocampus of the brain tissue, and enzyme-linked immunosorbent assay(ELISA)was employed to detect the content of TNF-α in the rat brain tissue. Results The number of TLR4 and NF-kB positive cells in the brain tissue of the TBI group and the TBI + searwater drowning group increased. The expressions of TLR4 and NF-kB mRNA in the hippocampus of the brain tissue of the TBI group and the TBI + SWD group significantly increased 3 hours after establishment of the TBI model. For the TBI group, the expressions of TLR4 and NF-kB were respectively (1.63±0.52) and (1.52±0.41), while in the the TBI + SWD group, the expressions of the above 2 substantce were respectively (4 1.87±0.93) and (1.87±0.93). At hour 24, the expression reached peak. For the TBI group, the expressions of TLR4 and NF-kB were respectively (49.61±0.34) and (4.60±0.51), while for the the TBI + SWD group, the expressions of the above 2 substantces were respectively (16.11±0.49) and (5.80±0.52), then they decreased gradually. The expression levels of TNF-α in the TBI group and the TBI + SWD group were found to elevate 3 hours after establishment of the model. TNF-α expression level for the TBI group was (53.68±1.48) ng/L), while the expression level of the same substance for the TBI + SWD group was (60.14±2.06) ng/L. Wave peak appeared at hour 12, and the wave peak for the TBI group was (79.28±2.46) ng/L, while for the TBI + SWD group, it displayed at (103.51±5.53) ng/L. Conclusion Seawater drowning could aggravate nerve inflammatory response mediated by TLR4/NF-kB signal pathway, which might play an important role in the rat brain injury induced by trauma. Key words: Traumatic brain injury; Seawater drowning; TLR4; NF-kB; TNF-α