Background: The aim of this study was to investigate the efficacy of hyperbaric oxygen in secondary brain injury after trauma and its mechanism in a rat model.
Material/Methods: A rat model of TBI was constructed using the modified Feeney’s free-fall method, and 60 SD rats were random-ly divided into three groups – the sham group, the untreated traumatic brain injury (TBI) group, and the hyper-baric oxygen-treated TBI group. The neurological function of the rats was evaluated 12 and 24 hours after TBI modeling; the expression levels of TLR4, IkB, p65, and cleaved caspase-3 in the peri-trauma cortex were deter-mined by Western blot; levels of TNF-a, IL-6, and IL-1b were determined by ELISA; and apoptosis of the neurons was evaluated by TUNEL assay 24 hours after TBI modeling.
Results: Hyperbaric oxygen therapy significantly inhibited the activation of the TLR4/NF-kB signaling pathway, reduced the expression of cleaved caspase-3, TNF-a, IL-6 and IL-1b (P<0.05), reduced apoptosis of the neurons and improved the neurological function of the rats (P<0.05).
Conclusions: Hyperbaric oxygen therapy protects the neurons after traumatic injury, possibly through inhibition of the TLR4/ NF-kB signaling pathway.