Hypertonic saline improves brain edema resulting from traumatic brain injury by suppressing the NF-κB/IL-1β signaling pathway and AQP4.

Although hypertonic saline (HS) has been extensively applied to treat brain edema in the clinic, the precise mechanism underlying its function remains poorly understood. Therefore, the aim of the present study was to investigate the therapeutic mechanism of HS in brain edema in terms of aquaporins and inflammatory factors. In the present study, traumatic brain injury (TBI) was established in male adult Sprague-Dawley rats, which were continuously administered 10% HS by intravenous injection for 2 days. In addition, brain edema and brain water content were detected by MRI and wet/dry ratio analysis and histological examination, respectively. Immunohistochemical staining for albumin and western blotting for occludin, zonula occludens-1 and claudin-5 was performed to evaluate the integrity of the blood-brain barrier. Aquaporin 4 (AQP4) expression was also analyzed using western blotting and reverse transcription-quantitative PCR, whilst interleukin (IL)-1β and NF-κB levels were measured using ELISA. It was demonstrated that HS treatment significantly reduced brain edema in TBI rats and downregulated AQP4 expression in cerebral cortical tissues around the contusion site. In addition, IL-1β and NF-κB levels were found to be downregulated after 10% HS treatment. Therefore, results from the present study suggested that HS may protect against brain edema induced by TBI by modulating the expression levels of AQP4, NF-κB and IL-1β.