title: Hyperbaric Oxygen Intervention Modulates Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats: Possible Involvement of TLR4/NF-x03BA; B-Mediated Signaling Pathway.
abstract: OBJECTIVE
  Previous studies have proved that the activation of TLR4/NF-x03BA; B signaling pathway is involved in inflammatory processes in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Hyperbaric oxygen (HBO) intervention has successfully been used to treat several animal models of tissue injury via its anti-inflammation property. This study was undertaken to investigate the influence of HBO administration on the TLR4/NF-x03BA; B signaling pathway in rats at the early stage of SAH.
  
  
  METHODS
  Male Sprague-Dawley rats (n = 150) were randomly divided into 5 groups: the sham, the sham + 2.8 atmospheres absolute (ATA) HBO group, the SAH group, the SAH + 2.0ATA HBO group, the SAH + 2.8ATA HBO group. Each group (n = 30) was randomly subdivided into three subgroups that were examined at the following time points: 24 h, 48 h and 72 h post-injury. HBO (100% O2, 2.0ATA or 2.8ATA for 90mins) was initiated 12 h after injury. Neurological deficit, brain edema and blood-brain barrier (BBB) permeability were assessed to evaluate the development of EBI. The expressions of TLR4, NF-x03BA; B and pro-inflammatory cytokines in the cortical were determined by real time polymerase chain reaction (RT-PCR), western blot, immunohistochemistry, or enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  Our study showed that treatment with HBO significantly decreased the expressions of TLR4, NF-x03BA; B and the downstream inflammatory agents, such as TNF-α, IL-6, IL-1β and ICAM-1, and also improved brain edema, blood-brain barrier permeability and neurologic function.
  
  
  CONCLUSIONS
  These findings indicate that HBO treatment may result in abatement of the development of EBI after SAH, possibly through suppression of TLR4/NF-x03BA; B signaling pathway.
authors.forename: Hao
authors.initials: H
authors.lastname: Liu
authors.forename: Ming
authors.initials: M
authors.lastname: Yang
authors.forename: Li
authors.initials: L
authors.lastname: Pan
authors.forename: Peng
authors.initials: P
authors.lastname: Liu
authors.forename: Lianting
authors.initials: L
authors.lastname: Ma
mesh_terms: D000818:Animals; D001921:Brain / Q000276:immunology / Q000473:pathology; D001930:Brain Injuries / Q000209:etiology* / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D006931:Hyperbaric Oxygenation / Q000379:methods; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology; D008297:Male; D016328:NF-kappa B / Q000276:immunology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D051197:Toll-Like Receptor 4 / Q000276:immunology*
chemical_list: D016328:NF-kappa B; D051197:Toll-Like Receptor 4; D018799:Intercellular Adhesion Molecule-1