Hyperbaric oxygen alleviates the activation of NLRP‑3‑inflammasomes in traumatic brain injury
- Huihui Qian
- Qinghe Li
- Woda Shi
Affiliations: Department of Geriatrics, The Affiliated Yancheng Hospital, Southeast University Medical College, Yancheng, Jiangsu 224001, P.R. China, Department of Nursing, The Affiliated Yancheng Hospital, Southeast University Medical College, Yancheng, Jiangsu 224001, P.R. China, Department of Cardiothoracic Surgery, The Affiliated Yancheng Hospital, Southeast University Medical College, Yancheng, Jiangsu 224001, P.R. China
- Published online on: July 24, 2017 https://doi.org/10.3892/mmr.2017.7079
Copyright: © Qian
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Growing evidence has demonstrated that the nucleotide‑binding oligomerization domain‑like receptor family pyrin domain containing 3 (NLRP‑3) inflammasome‑mediated inflammatory pathways have been involved in the secondary injury of traumatic brain injury (TBI). In the present study, the authors investigated the effects of hyperbaric oxygen (HBO) therapy on the NLRP‑3 inflammasome pathway following TBI. Following the evaluation of motor deficits and brain edema, the therapeutic effects of HBO on interleukin (IL)‑1β and IL‑18 expression were assessed, as well as NLRP‑3 inflammasome activation following TBI. HBO may improve motor score and reduce brain edema, accompanied with the reduction of IL‑1β and IL‑18 during the 7‑day observation period. Furthermore, HBO suppressed mRNA and protein expression of NLRP‑3‑inflammasome components, especially reducing NLRP‑3 expression in microglia. Thus, these results suggested that HBO alleviates the inflammatory response in experimental TBI via modulating microglial NLRP‑3‑inflammasome signaling.