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

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

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Department of Neurosurgery, Liaocheng People's Hospital, Liaocheng, PR China.



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.


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.


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.


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

[Indexed for MEDLINE]

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