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@ARTICLE{Liu:906462,
      author       = {Liu, Jingjin and Veldeman, Michael and Höllig, Anke and
                      Nolte, Kay and Liebenstund, Lisa and Willuweit, Antje and
                      Langen, Karl-Josef and Rossaint, Rolf and Coburn, Mark},
      title        = {{P}ost-stroke treatment with argon preserved neurons and
                      attenuated microglia/macrophage activation long-termly in a
                      rat model of transient middle cerebral artery occlusion
                      (t{MCAO})},
      journal      = {Scientific reports},
      volume       = {12},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {FZJ-2022-01465},
      pages        = {691},
      year         = {2022},
      abstract     = {In a previous study from our group, argon has shown to
                      significantly attenuate brain injury, reduce brain
                      inflammation and enhance M2 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.},
      cin          = {INM-4},
      ddc          = {600},
      cid          = {I:(DE-Juel1)INM-4-20090406},
      pnm          = {5253 - Neuroimaging (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5253},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {35027642},
      UT           = {WOS:000742412100008},
      doi          = {10.1038/s41598-021-04666-x},
      url          = {https://juser.fz-juelich.de/record/906462},
}