Post-stroke treatment with argon preserved neurons and attenuated microglia/macrophage activation long-termly in a rat model of transient middle cerebral artery occlusion (tMCAO)

• Published in: Scientific reports Vol. 12; no. 1; pp. 691 - 12
• Main Authors: Liu, Jingjin, Veldeman, Michael, Höllig, Anke, Nolte, Kay, Liebenstund, Lisa, Willuweit, Antje, Langen, Karl-Josef, Rossaint, Rolf, Coburn, Mark
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 13.01.2022; Nature Publishing Group; Nature Portfolio
• Subjects: 692/699/375/534; 692/700/565; Age; Anesthesiology; Animals; Argon; Argon - administration & dosage; Argon - pharmacology; Biological analysis; Blood pressure; Brain injury; Cell activation; Cerebral blood flow; Disease Models, Animal; Heart rate; Hospitals; Humanities and Social Sciences; Infarction, Middle Cerebral Artery - drug therapy; Infarction, Middle Cerebral Artery - immunology; Ischemia; Long-term effects; Macrophage Activation - drug effects; Macrophages; Microglia; multidisciplinary; Neuroprotection; Neuroprotective Agents; Quantitative analysis; Rats; Reperfusion; Science; Science (multidisciplinary); Sensorimotor system; Stroke; Time Factors; Time-to-Treatment; Variance analysis; Veins & arteries
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-021-04666-x

In a previous study from our group, argon has shown to significantly attenuate brain injury, reduce brain inflammation and enhance M 2 microglia/macrophage polarization until 7 days after ischemic stroke. However, the long-term effects of argon have not been reported thus far. In the present study, we analyzed the underlying neuroprotective effects and potential mechanisms of argon, up to 30 days after ischemic stroke. Argon administration with a 3 h delay after stroke onset and 1 h after reperfusion demonstrated long-term neuroprotective effect by preserving the neurons at the ischemic boundary zone 30 days after stroke. Furthermore, the excessive microglia/macrophage activation in rat brain was reduced by argon treatment 30 days after ischemic insult. However, long-lasting neurological improvement was not detectable. More sensorimotor functional measures, age- and disease-related models, as well as further histological and molecular biological analyses will be needed to extend the understanding of argon’s neuroprotective effects and mechanism of action after ischemic stroke.