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Post-stroke treatment with argon shown to alleviate brain injury in rats

05 June 2019

Jingjin Liu, Kay Nolte, Gary Brook, Lisa Liebenstund, Agnieszka Weinandy, Anke Höllig, Michael Veldeman, Antje Willuweit, Karl-Josef Langen, Rolf Rossaint and Mark Coburn

Stroke has become one of the most frequent causes of death as well as a leading cause of major disability worldwide1.

In recent years, argon has been shown to exert neuroprotective effects in both in vitro and in vivo models and has significant implications in relation to the treatmentof ischemic stroke patients. Although the mechanisms by which argon exerts its neuroprotective characteristics remain unclear, accumulating evidence implies that argon may exert neuroprotective effects via modulating the activation and polarization of microglia/macrophages after ischemic stroke. In this study, using twenty-one male Wistar rats, the underlying neuroprotective effects of delayed argon application were analysed up to 7 days after reperfusion and the potential mechanisms involved were explored.

It was found that, when argon was administered with a 3 h delay after stroke onset and 1 h after reperfusion, neurological deficit was significantly alleviated within the first week and the neurons at the ischemic boundary zone were found to be preserved 7 days after stroke. Moreover, argon reduced the excessive microglia/macrophage activation and promoted the switch of microglia/macrophage polarization towards the anti-inflammatory M2 phenotype.

Given that argon has no record of toxicity2,3,4, and could exert neuroprotection via multiple mechanisms, it is a promising agent for treating ischemic stroke patients in the future.

Original publication:

Post-stroke treatment with argon attenuated brain injury, reduced brain inflammation and enhanced M2 microglia/macrophage polarization: a randomized controlled animal study


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2 Zhao H, Mitchell S, Ciechanowicz S, Savage S, Wang T, Ji X, Ma D. Argon protects against hypoxic-ischemic brain injury in neonatal rats through activation of nuclear factor (erythroid-derived 2)-like 2. Oncotarget. 2016; 7(18):25640-51

3 Gardner AJ, Menon DK. Moving to human trials for argon neuroprotection in neurological injury: a narrative review. Br J Anaesth. 2018;120(3):453–68

4 Ulbrich F, Goebel U. The molecular pathway of argon-mediated neuroprotection. Int J Mol Sci. 2016;17(11)