Attenuating inflammation but stimulating both angiogenesis and neurogenesis using hyperbaric oxygen in rats with traumatic brain injury

Abstract

Collectively, these results suggest that HBO2 therapy may improve outcomes of TBI in rats by inhibiting activated inflammation and gliosis while stimulating both angiogenesis and neurogenesis in the early stage.

Hyperbaric oxygen therapy (HBOT) suppresses biomarkers of cell stress and kidney injury in diabetic mice

“…HBOT can attenuate inflammatory responses by altering cytokine production and signaling (Alex et al 2005;Daniel et al 2011;Lin et al 2012). The anti-inflammatory action of HBOT may arise in part from its ability to increase the expression of antioxidant genes and other cellular defense genes through the induction of a noncytotoxic oxidative stimulus (Matsunami et al 2009(Matsunami et al , 2011Simsek et al 2011;Godman et al 2010a, b;He et al 2011).…”

Reflections on the neurotherapeutic effects of hyperbaric oxygen

“…HBOT is a treatment in which oxygen-enriched air (up to 100%) is administrated to patients in a chamber where the pressure is elevated above one atmosphere absolute (1ATA), which is the ambient atmospheric pressure). It is becoming widely acknowledged that the combined action of hyperoxia and hyperbaric pressure leads to significant improvement in tissue oxygenation while targeting both oxygenand pressure-sensitive genes [3][4][5][6], resulting in improved mitochondrial metabolism with anti-apoptotic and anti-inflammatory effects [7][8][9][10][11][12].…”

“…At the cellular level, HBOT can improve cellular metabolism, reduce apoptosis, alleviate oxidative stress and increase levels of neurotrophins and nitric oxide through enhancement of mitochondrial function in both neurons and glial cells, and may even promote neurogenesis of endogenous neural stem cells [7][8][9][10][11][12]14]. Regarding mitochondria, it is important to note that stroke and TBI engender depolarization of the mitochondria membrane and induction of mitochondrial permeability transition pore, which reduces the efficiency of energy production and elevate the level of reactive oxygen species [15].…”

“…The decreased oxygen level not only causes reduction in neuronal activity but also prevents the generation of new synaptic connections and angiogenesis. HBOT can initiate vascular repair and improve cerebral vascular flow, induce regeneration of axonal white matter, stimulate axonal growth, promote blood-brain barrier integrity and reduce inflammatory reactions as well as brain edema [7][8][9][10][11][12].…”

“…However, this will require novel basic biomedical research to understand the HBOT effect on the recently discovered mitochondria-associated cellular response to hypoxia [7][8][9][10][11][12], which is a common denominator of stroke, TBI, dementia and aging [25,26].…”