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@ARTICLE{Bernis:271140,
      author       = {Bernis, Maria E. and Hakvoort, Charlotte and Nacarkucuk,
                      Efe and Burkard, Hannah and Bremer, Anna-Sophie and Zweyer,
                      Margit and Maes, Elke and Grzelak, Kora A. and Sabir,
                      Hemmen},
      title        = {{N}europrotective {E}ffect of {C}lemastine {I}mproved
                      {O}ligodendrocyte {P}roliferation through the {MAPK}/{ERK}
                      {P}athway in a {N}eonatal {H}ypoxia {I}schemia {R}at
                      {M}odel},
      journal      = {International journal of molecular sciences},
      volume       = {25},
      number       = {15},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DZNE-2024-01008},
      pages        = {8204},
      year         = {2024},
      abstract     = {Neonatal hypoxic-ischemic encephalopathy is the most common
                      cause of long-term disability in term neonates, and white
                      matter injury is the primary cause of cerebral palsy.
                      Therapies that focus on the neuroprotection of myelination
                      and oligodendrocyte proliferation could potentially
                      ameliorate long-lasting neurological impairments after
                      hypoxic-ischemic encephalopathy. Clemastine, a histamine H1
                      antagonist, has been shown to exert neuroprotective effects
                      in multiple sclerosis and spinal cord injury by promoting
                      oligodendrogenesis and re-myelination. In this study, we
                      demonstrated the neuroprotective effects of clemastine in
                      our rat model of neonatal hypoxic-ischemic brain injury.
                      Animals received a single intraperitoneal injection of
                      either vehicle or clemastine (10 mg/kg) for 6 consecutive
                      days. Our results showed a significant reduction in white
                      matter loss after treatment, with a clear effect of
                      clemastine on oligodendrocytes, showing a significant
                      increase in the number of Olig2+ cells. We characterized the
                      MAPK/ERK pathway as a potential mechanistic pathway
                      underlying the neuroprotective effects of clemastine.
                      Altogether, our results demonstrate that clemastine is a
                      potential compound for the treatment of hypoxic-ischemic
                      encephalopathy, with a clear neuroprotective effect on white
                      matter injury by promoting oligodendrogenesis.},
      keywords     = {Animals / Oligodendroglia: drug effects / Oligodendroglia:
                      metabolism / Neuroprotective Agents: pharmacology /
                      Neuroprotective Agents: therapeutic use / Hypoxia-Ischemia,
                      Brain: drug therapy / Hypoxia-Ischemia, Brain: metabolism /
                      Hypoxia-Ischemia, Brain: pathology / Rats / Clemastine:
                      pharmacology / MAP Kinase Signaling System: drug effects /
                      Animals, Newborn / Disease Models, Animal / Cell
                      Proliferation: drug effects / Rats, Sprague-Dawley},
      cin          = {AG Sabir},
      ddc          = {540},
      cid          = {I:(DE-2719)5000032},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39125778},
      pmc          = {pmc:PMC11311837},
      doi          = {10.3390/ijms25158204},
      url          = {https://pub.dzne.de/record/271140},
}