title: Hyperbaric Oxygen Alleviates Secondary Brain Injury After Trauma Through Inhibition of TLR4/NF-κB Signaling Pathway.
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.
  
  
  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.
authors.affiliation: Department of Hyperbaric Oxygen, Navy General Hospital, Beijing, China (mainland).
authors.forename: Xiang-En
authors.initials: XE
authors.lastname: Meng
authors.affiliation: Department of Hyperbaric Oxygen, Navy General Hospital, Beijing, China (mainland).
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Hyperbaric Oxygen, Navy General Hospital, Beijing, China (mainland).
authors.forename: Na
authors.initials: N
authors.lastname: Li
authors.affiliation: Department of Hyperbaric Oxygen, Navy General Hospital, Beijing, China (mainland).
authors.forename: Dan-Feng
authors.initials: DF
authors.lastname: Fan
authors.affiliation: Department of Hyperbaric Oxygen, Navy General Hospital, Beijing, China (mainland).
authors.forename: Chen
authors.initials: C
authors.lastname: Yang
authors.affiliation: Department of Hyperbaric Oxygen, Navy General Hospital, Beijing, China (mainland).
authors.forename: Hang
authors.initials: H
authors.lastname: Li
authors.affiliation: Department of Hyperbaric Oxygen, Navy General Hospital, Beijing, China (mainland).
authors.forename: Da-Zhi
authors.initials: DZ
authors.lastname: Guo
authors.affiliation: Department of Hyperbaric Oxygen, Navy General Hospital, Beijing, China (mainland).
authors.forename: Shu-Yi
authors.initials: SY
authors.lastname: Pan
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001930:Brain Injuries / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D053148:Caspase 3 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D006931:Hyperbaric Oxygenation; D020672:I-kappa B Proteins / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D010100:Oxygen / Q000494:pharmacology; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D051197:Toll-Like Receptor 4 / Q000378:metabolism*; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D016207:Cytokines; D020672:I-kappa B Proteins; D016328:NF-kappa B; D051197:Toll-Like Receptor 4; D051996:Transcription Factor RelA; D053148:Caspase 3; D010100:Oxygen
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