We investigated the effects of hyperbaric
oxygen treatment on the Nrf2 signaling pathway in secondary injury following
traumatic brain injury, using a rat model. An improved Feeney freefall method was used to establish the rat
traumatic brain injury model. Sixty rats were randomly divided into three groups: a
sham surgery group, a
traumatic brain injury group, and a group receiving hyperbaric
oxygen treatment after
traumatic brain injury. Neurological function scores were assessed at 12 and 24 h after injury. The expression levels of Nrf2,
heme oxygenase 1 (HO-1), and
quinine oxidoreductase 1 (NQO-1) in the cortex surrounding the brain lesion were detected by western blotting 24 h after the injury. Additionally, the TUNEL method was used to detect apoptosis of nerve cells 24 h after traumatic injury and Nissl staining was used to detect the number of whole neurons. Hyperbaric
oxygen treatment significantly increased the expression of nuclear Nrf2
protein (P < 0.05), HO-1, and NQO-1 in the brain tissues surrounding the lesion after a
traumatic brain injury (P < 0.05) and also significantly reduced the number of apoptotic and injured nerve cells. The neurological function scores also improved with hyperbaric
oxygen treatment (P < 0.05). Therefore, hyperbaric
oxygen has a neuroprotective role in
traumatic brain injury, which is mediated by up-regulation of the Nrf2 signaling pathway.