Argon gas: a potential neuroprotectant and promising medical therapy

Abstract

Argon is a noble gas element that has demonstrated narcotic and protective abilities that may prove useful in the medical field. The earliest records of argon gas have exposed its ability to exhibit narcotic symptoms at hyperbaric pressures greater than 10 atmospheres with more recent evidence seeking to display argon as a potential neuroprotective agent. The high availability and low cost of argon provide a distinct advantage over using similarly acting treatments such as xenon gas. Argon gas treatments in models of brain injury such as in vitro Oxygen-Glucose-Deprivation (OGD) and Traumatic Brain Injury (TBI), as well as in vivo Middle Cerebral Artery Occlusion (MCAO) have largely demonstrated positive neuroprotective behavior. On the other hand, some warning has been made to potential negative effects of argon treatments in cases of ischemic brain injury, where increases of damage in the sub-cortical region of the brain have been uncovered. Further support for argon use in the medical field has been demonstrated in its use in combination with tPA, its ability as an organoprotectant, and its surgical applications. This review seeks to summarize the history and development of argon gas use in medical research as mainly a neuroprotective agent, to summarize the mechanisms associated with its biological effects, and to elucidate its future potential.

Figure 1

Commonly used ischemic models of neuroprotection. (A) An OGD model of neuroprotection places brain tissue into a medium that deprives it of oxygen and glucose in vitro. (B) The TBI model uses an apparatus to cause a forceful impact on the brain and results in ischemic tissue damage with treatments possible in vivo or in vitro. (C) The MCAO model ligates the middle cerebral artery to produce an ischemic infarction with treatments examined in vivo.

Figure 2

Theorized argon neuroprotective pathways. Suggested pathways still under investigation that may contribute to the neuroprotective effects of argon gas treatments in neuron cells include: NMDA receptor inhibition, direct stimulation of the MEK and ERK 1/2 anti-apoptotic pathway, and stimulation GABA_A receptor.