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

Abstract

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-α), transforming growth-interacting factor (TGIF), and TGF-β1 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% O₂ at one absolute atmosphere), TBI + HBO, and sham-operated normobaric air. The TBI + HBO rats received 100% O₂ at 2.0 absolute atmosphere for 1 h immediately after TBI. Local and systemic TNF-α expression, neuropathology, levels of the neuronal apoptosis-associated proteins TGIF and TGF-β1, 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-α 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-β1 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-α production, resulting in neuroprotective effects. We also suggest that decreased levels of TGIF and increased levels of TGF-β in the injured cortex leading to decreased neuronal apoptosis is one mechanism by which functional recovery may occur.

Keywords: Apoptosis; Hyperbaric oxygen therapy; Transforming growth factor-beta1; Transforming growth-interacting factor; Traumatic brain injury; Tumor necrosis factor-alpha.