Abstract

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 AND METHODS: A rat model of TBI was constructed using the modified Feeney’s free-fall method, and 60 SD rats were randomly divided into three groups – the sham group, the untreated traumatic brain injury (TBI) group, and the hyperbaric oxygen-treated TBI group. The neurological function of the rats was evaluated 12 and 24 hours after TBI modeling; the expression levels of TLR4, IκB, p65, and cleaved caspase-3 in the peri-trauma cortex were determined by Western blot; levels of TNF-α, IL-6, and IL-1β 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-κB signaling pathway, reduced the expression of cleaved caspase-3, TNF-α, IL-6 and IL-1β (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-κB signaling pathway.

Keywords: Apoptosis - drug effects, Animals, Brain Injuries - therapy, Caspase 3 - metabolism, Cytokines - metabolism, Hyperbaric Oxygenation, I-kappa B Proteins - metabolism, In Situ Nick-End Labeling, NF-kappa B - metabolism, Neurons - pathology, Oxygen - pharmacology, Rats, Sprague-Dawley, Signal Transduction - drug effects, Toll-Like Receptor 4 - metabolism, Transcription Factor RelA - metabolism