Effects of Hyperbaric Oxygen Therapy on Inflammasome Signaling after Traumatic Brain Injury

Neuroimmunomodulation. 2016;23(2):122-9. doi: 10.1159/000445689. Epub 2016 May 24.


Objective: Neuroinflammation plays an important role in secondary tissue damage after traumatic brain injury (TBI). Recently, the inflammasome-mediated inflammatory pathway has been observed in the inflammatory response of TBI. In this study, we investigated the influence of hyperbaric oxygen therapy (HBOT) on inflammasome activation after TBI.

Methods: The experimental mice were randomly divided into 4 groups as follows: sham-operated normobaric air (21% O2 at one absolute atmosphere), HBOT only, TBI + normobaric air and TBI + HBOT. Following the evaluation of motor deficits and brain edema, the expression of inflammasome components and effectors was measured by qRT-PCR and Western blotting. Moreover, alterations in IL-1β, IL-18 and high-mobility group box 1 (HMGB1) were calculated by enzyme-linked immunosorbent assay at each time point after injury.

Results: HBOT improved motor score and reduced brain edema. Furthermore, it suppressed protein expression of inflammasome components and reduced the levels of IL-1β and IL-18, accompanied by the reduction of HMGB1 in brain tissues and serum.

Conclusion: These results suggest that HBOT may alleviate the inflammatory response after TBI by inhibiting the activation of inflammasome signaling.

MeSH terms

  • Animals
  • Brain Injuries, Traumatic / metabolism*
  • Brain Injuries, Traumatic / therapy*
  • Hyperbaric Oxygenation / methods*
  • Hyperbaric Oxygenation / trends
  • Inflammasomes / physiology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Motor Activity / physiology
  • Random Allocation
  • Signal Transduction / physiology*
  • Treatment Outcome


  • Inflammasomes