Hyperbaric oxygen effects on neuronal apoptosis associations in a traumatic brain injury rat model

Background: The neuroprotective mechanisms of hyperbaric oxygen (HBO) therapy on traumatic brain injury (TBI) remain unclear, especially neuronal apoptosis associations such as the expression of tumor necrosis factor alpha (TNF-alpha), transforming growthinteracting factor (TGIF), and TGF-beta 1 after TBI. The aim of this study was to investigate the neuroprotective effects of HBO therapy in a rat model of TBI. Materials and methods: The experimental rats were randomly divided into three groups as follows: TBI + normobaric air (21% O-2 at one absolute atmosphere), TBI + HBO, and shamoperated normobaric air. The TBI + HBO rats received 100% O-2 at 2.0 absolute atmosphere for 1 h immediately after TBI. Local and systemic TNF-alpha expression, neuropathology, levels of the neuronal apoptosis-associated proteins TGIF and TGF-beta 1, and functional outcome were evaluated 72 h after the onset of TBI. Results: Compared to the TBI control groups, the running speed of rats on the TreadScan after TBI was significantly attenuated by HBO therapy. The TBI-induced local and systemic TNF-alpha expression, neuronal damage score, and neuronal apoptosis were also significantly reduced by HBO therapy. Moreover, HBO treatment attenuated the expression of TGIF but increased TGF-beta 1 expression in neurons. Conclusions: We concluded that treatment of TBI with HBO during the acute phase of injury can decrease local and systemic proinflammatory cytokine TNF-alpha production, resulting in neuroprotective effects. We also suggest that decreased levels of TGIF and increased levels of TGF-beta in the injured cortex leading to decreased neuronal apoptosis is one mechanism by which functional recovery may occur. (C) 2015 Elsevier Inc. All rights reserved.