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. 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. 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). Hyperbaric oxygen therapy protects the neurons after traumatic injury, possibly through inhibition of the TLR4/NF-κB signaling pathway.
Meng, Zhang, Li, Fan, Yang, Li, Guo, Pan, (2016). Hyperbaric Oxygen Alleviates Secondary Brain Injury After Trauma Through Inhibition of TLR4/NF-κB Signaling Pathway. Medical science monitor : international medical journal of experimental and clinical research, 2016 Jan;22():284-8. https://www.ncbi.nlm.nih.gov/pubmed/26812205